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PURPOSE: The purpose of this study was to understand potential baseline transcriptional expression differences in paraspinal skeletal muscle from patients with different underlying lumbar pathologies by comparing multifidus gene expression profiles across individuals with either disc herniation, facet arthropathy, or degenerative spondylolisthesis. METHODS: Multifidus biopsies were obtained from patients (n = 44) undergoing lumbar surgery for either disc herniation, facet arthropathy, or degenerative spondylolisthesis. Diagnostic categories were based on magnetic resonance images, radiology reports, and intraoperative reports. Gene expression for 42 genes was analysed using qPCR. A one-way analysis of variance was performed for each gene to determine differences in expression across diagnostic groups. Corrections for multiple comparisons across genes (Benjamini-Hochberg) and for between-group post hoc comparisons (Sidak) were applied. RESULTS: Adipogenic gene (ADIPOQ) expression was higher in the disc herniation group when compared to the facet arthropathy group (p = 0.032). Adipogenic gene (PPARD) expression was higher in the degenerative spondylolisthesis group when compared to the disc herniation group (p = 0.013), although absolute gene expression levels for all groups was low. Fibrogenic gene (COL3A1) had significantly higher expression in the disc herniation group and facet arthropathy group when compared to the degenerative spondylolisthesis group (p

A common animal model of muscle pathology following rotator cuff tear (RCT) is a tenotomy of the supraspinatus and infraspinatus, often combined with neurotomy of the suprascapular nerve, which induces a more robust atrophy response than tenotomy alone. However, the utility of this model depends on its similarity to human muscle pathology post‐RCT, both in terms of the disease phenotype and mechanisms of muscle atrophy and fatty infiltration. Given the clinical prevalence of nerve injury is low and the muscular response to denervation is distinct from mechanical unloading in other models, an understanding of the biological influence of the nerve injury is critical for interpreting data from this RCT model. We evaluated the individual and combined effect of tenotomy and neurotomy across multiple biological scales, in a robust time‐series in the mouse supraspinatus. Muscle composition, histological, and gene expression data related to muscle atrophy, degeneration–regeneration, fatty infiltration, and fibrosis were evaluated. Broadly, we found tenotomy alone caused small, transient changes in these pathological features, which resolved over the course of the study, while neurotomy alone caused a significant fatty atrophy phenotype. The dual injury group had a similar fatty atrophy phenotype to the neurotomy group, though the addition of tenotomy did marginally enhance the fat and connective tissue. Overall, these results suggest the most clinically relevant injury model, tenotomy alone, does not produce a clinically relevant phenotype. The dual injury model partially recapitulates the human condition, but it does so through a nerve injury, which is not well justified clinically. [ABSTRACT FROM AUTHOR]

Fatty infiltration of the rotator cuff muscles is very common following rotator cuff tears and is one of the most important factors in determining treatment. Current clinical practice relies on subjective evaluation of fatty infiltration through categorical scoring based on the Goutallier classification system. The Dixon magnetic resonance imaging (MRI) sequence provides flexibility in selecting echo times for water–fat separation. The Dixon method, therefore, has the potential to provide robust and high-quality fat quantification that allows for more accurate calculation of fat fraction (%Fat) of the rotator cuff muscles than the Goutallier classification system. However, significant variance exists in sequencing and post-processing methodology within the recent application of Dixon sequences to quantify rotator cuff fatty infiltration. In this paper, we conducted a systematic review to synthesize the relevant literature utilizing Dixon sequencing for the quantification of rotator cuff fatty infiltration. The literature search was extracted from 1094 articles, with 12 studies included in the final review. Regardless of the varying sequencing pattern and post-processing techniques among studies, the findings suggest the Dixon method is reliable for quantitatively calculating the fat fraction of the rotator cuff muscles, even at very low levels of fatty infiltration. In addition, a quantitative difference in fat fraction was observed between participants with different degrees of tear vs. those without any shoulder pathologies. Multi-point Dixon imaging has the potential to be utilized clinically to objectively quantify fatty infiltration and may lead to improved clinical decision making for patients with rotator cuff tears. [ABSTRACT FROM AUTHOR]

Background: Patients treated for symptomatic rotator cuff tear (RCT) on one shoulder seem to have a higher prevalence of RCT on the contralateral shoulder. Purpose: To compare the supraspinatus (SSP) tendon and RC muscle properties on the contralateral shoulder in patients after repair surgery to those healthy individuals using quantitative magnetic resonance imaging (MRI). Material and Methods: A total of 23 patients treated for RCT (group A) and 23 healthy controls (group B) were recruited. Constant score, visual analog scale score (VAS), and MRI examinations were conducted. The SSP tendon structural status was graded based on the Zlatkin classification and quantified on ultrashort echo time (UTE)-T2* mapping images. Fatty degeneration of RC muscles was classified according to the Goutallier classification and quantified on T2 mapping. Results: The Constant and VAS scores were comparable between groups A and B (all P >0.05). No significant differences were observed in tendon structural status between the two groups (P >0.05). However, significant differences were established in UTE-T2* values of the SSP tendon on the distal subregion between groups A and B (16.4 ± 2.4 ms vs. 14.8 ± 1.2 ms; P = 0.01). Regarding muscle degeneration, no significant differences were displayed in T2 values and Goutallier classification of RC muscles (all P >0.05). Conclusion: Patients with a treated RCT demonstrated inferior SSP tendon in the distal subregion on the contralateral shoulders one year postoperatively compared to that of healthy controls based on quantitative MRI data. [ABSTRACT FROM AUTHOR]

Aims: Rotator cuff (RC) injuries are characterized by tendon rupture, muscle atrophy, retraction, and fatty infiltration, which increase injury severity and jeopardize adequate tendon repair. Epigenetic drugs, such as histone deacetylase inhibitors (HDACis), possess the capacity to redefine the molecular signature of cells, and they may have the potential to inhibit the transformation of the fibro-adipogenic progenitors (FAPs) within the skeletal muscle into adipocyte-like cells, concurrently enhancing the myogenic potential of the satellite cells. Methods: HDACis were added to FAPs and satellite cell cultures isolated from mice. The HDACi vorinostat was additionally administered into a RC injury animal model. Histological analysis was carried out on the isolated supra- and infraspinatus muscles to assess vorinostat anti-muscle degeneration potential. Results: Vorinostat, a HDACi compound, blocked the adipogenic transformation of muscle-associated FAPs in culture, promoting myogenic progression of the satellite cells. Furthermore, it protected muscle from degeneration after acute RC in mice in the earlier muscle degenerative stage after tenotomy. Conclusion: The HDACi vorinostat may be a candidate to prevent early muscular degeneration after RC injury. Cite this article: Bone Joint Res 2024;13(4):169–183.

Background: Muscle edema formation and inflammatory processes are early manifestations of acute rotator cuff lesions in sheep. Histological analysis of affected muscles revealed edema formation, inflammatory changes, and muscle tissue disruption in MRs. Hypothesis: Edema contributes to inflammatory reactions and early muscle fiber degeneration before the onset of fatty infiltration. Study Design: Controlled laboratory study. Methods: Osteotomy of the greater tuberosity, including the insertion of the infraspinatus tendon, was performed on 14 sheep. These experimental animal models were divided into 2 groups: a nontrauma group with surgical muscle release alone (7 sheep) and a trauma group with standardized application of additional trauma to the musculotendinous unit (7 sheep). Excisional biopsy specimens of the infraspinatus muscle were taken at 0, 3, and 4 weeks. Results: Edema formation was histologically demonstrated in both groups and peaked at 3 weeks. At 3 weeks, signs of muscle fiber degeneration were observed. At 4 weeks, ingrowth of loose alveolar and fibrotic tissue between fibers was detected. Fatty tissue was absent. The diameter of muscle fibers increased in both groups, albeit to a lesser degree in the trauma group, and practically normalized at 4 weeks. Immunohistology revealed an increase in macrophage types 1 and 2, as well as inflammatory mediators such as prostaglandin E2 and nuclear factor kappa-light-chain-enhancer of activated B cells. Conclusion: Early muscle edema and concomitant inflammation precede muscle fiber degeneration and fibrosis. Edema formation results from tendon release alone and is only slightly intensified by additional trauma. Clinical Relevance: This study illustrates that early edema formation and inflammation elicit muscle fiber degeneration that precedes fatty infiltration. Should this phenomenon be applicable to human traumatic rotator cuff tears, then surgery should be performed as soon as possible, ideally within the first 21 days after injury. [ABSTRACT FROM AUTHOR]

Fatty expansion is one of the features of muscle degeneration due to muscle injuries, and its presence interferes with muscle regeneration. Specifically, poor clinical outcomes have been linked to fatty expansion in rotator cuff tears and repairs. Our group recently found that fibroblast growth factor 8b (FGF-8b) inhibits adipogenic differentiation and promotes myofiber formation of mesenchymal stem cells in vitro. This led us to hypothesize that FGF-8b could similarly control the fate of muscle-specific cell populations derived from rotator cuff muscle involved in muscle repair following rotator cuff injury. In this study, we isolate fibro-adipogenic progenitor cells (FAPs) and satellite stem cells (SCs) from rat rotator cuff muscle tissue and analyzed the effects of FGF-8b supplementation. Utilizing a cell plating protocol, we successfully isolate FAPs-rich fibroblasts (FIBs) and SCs-rich muscle progenitor cells (MPCs). Subsequently, we demonstrate that FIB adipogenic differentiation can be inhibited by FGF-8b, while MPC myogenic differentiation can be enhanced by FGF-8b. We further demonstrate that phosphorylated ERK due to FGF-8b leads to the inhibition of adipogenesis in FIBs and SCs maintenance and myofiber formation in MPCs. Together, these findings demonstrate the powerful potential of FGF-8b for rotator cuff repair by altering the fate of muscle undergoing degeneration. [ABSTRACT FROM AUTHOR]

Aims: Rotator cuff muscle atrophy and fatty infiltration affect the clinical outcomes of rotator cuff tear patients. However, there is no effective treatment for fatty infiltration at this time. High-intensity interval training (HIIT) helps to activate beige adipose tissue. The goal of this study was to test the role of HIIT in improving muscle quality in a rotator cuff tear model via the β3 adrenergic receptor (β3AR). Methods: Three-month-old C57BL/6 J mice underwent a unilateral rotator cuff injury procedure. Mice were forced to run on a treadmill with the HIIT programme during the first to sixth weeks or seventh to 12th weeks after tendon tear surgery. To study the role of β3AR, SR59230A, a selective β3AR antagonist, was administered to mice ten minutes before each exercise through intraperitoneal injection. Supraspinatus muscle, interscapular brown fat, and inguinal subcutaneous white fat were harvested at the end of the 12th week after tendon tear and analyzed biomechanically, histologically, and biochemically. Results: Histological analysis of supraspinatus muscle showed that HIIT improved muscle atrophy, fatty infiltration, and contractile force compared to the no exercise group. In the HIIT groups, supraspinatus muscle, interscapular brown fat, and inguinal subcutaneous white fat showed increased expression of tyrosine hydroxylase and uncoupling protein 1, and upregulated the β3AR thermogenesis pathway. However, the effect of HIIT was not present in mice injected with SR59230A, suggesting that HIIT affected muscles via β3AR. Conclusion: HIIT improved supraspinatus muscle quality and function after rotator cuff tears by activating systemic sympathetic nerve fibre near adipocytes and β3AR. Cite this article: Bone Joint Res 2023;12(8):455–466.

Peripheral arterial disease (PAD) leads to chronic vascular occlusion and results in end organ damage in critically perfused limbs. There are currently no clinical methods available to determine the muscular damage induced by chronic mal-perfusion. This monocentric prospective cross-sectional study investigated n = 193 adults, healthy to severe PAD, in order to quantify the degree of calf muscle degeneration caused by PAD using a non-invasive hybrid ultrasound and single wavelength optoacoustic imaging (US/SWL-OAI) approach. While US provides morphologic information, SWL-OAI visualizes the absorption of pulsed laser light and the resulting sound waves from molecules undergoing thermoelastic expansion. US/SWL-OAI was compared to multispectral data, clinical disease severity, angiographic findings, phantom experiments, and histological examinations from calf muscle biopsies. We were able to show that synergistic use of US/SWL-OAI is most likely to map clinical degeneration of the muscle and progressive PAD.

Rotator cuff tears are a prevalent musculoskeletal problem that affect many individuals and may result in substantial social and health-related expenses. Moreover, the muscular fat infiltration and dystrophy associated with rotator cuff tears have been persistent challenges in rotator cuff surgical repair and postoperative rehabilitation. In this study, an in situ-formed injectable sodium alginate (SA) and bioglass (BG) hydrogel consisting of poly (lactic-co-glycolic acid) (PLGA) microspheres containing metformin (SA/BG-PLGA-Met) was developed for the prevention of muscular fat infiltration and dystrophy. Metformin and silicon ions were slowly released by the combined hydrogel, resulting in long-term biological effects. Moreover, the hydrogel displayed excellent degradability and biocompatibility. Extracts of SA/BG-PLGA-Met inhibited the adipogenesis of 3T3-L1 cells and stimulated the myogenic differentiation of C2C12 cells in vitro. In a mouse model of rotator cuff degeneration, the SA/BG-PLGA-Met hydrogel inhibited fat infiltration and dystrophy of the supraspinatus muscle. Overall, the SA/BG-PLGA-Met hydrogel, as a novel biomaterial, has great clinical potential for preventing rotator cuff muscle fat infiltration and atrophy.

Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant epigenetic disorder with highly variable muscle involvement and disease progression. Ongoing clinical trials, aimed at counteracting muscle degeneration and disease progression in FSHD patients, increase the need for reliable biomarkers. Muscle magnetic resonance imaging (MRI) studies showed that the appearance of STIR-positive (STIR+) lesions in FSHD muscles represents an initial stage of muscle damage, preceding irreversible adipose changes. Our study aimed to investigate fibrosis, a parameter of muscle degeneration undetectable by MRI, in relation to disease activity and progression of FSHD muscles. We histologically evaluated collagen in FSHD1 patients’ (STIR+ n = 27, STIR− n = 28) and healthy volunteers’ (n = 12) muscles by picrosirius red staining. All patients (n = 55) performed muscle MRI before biopsy, 45 patients also after 1 year and 36 patients also after 2 years. Fat content (T1 signal) and oedema/inflammation (STIR signal) were evaluated at baseline and at 1- and 2-year MRI follow-up. STIR+ muscles showed significantly higher collagen compared to both STIR− (p = 0.001) and healthy muscles (p < 0.0001). STIR− muscles showed a higher collagen content compared to healthy muscles (p = 0.0194). FSHD muscles with a worsening in fatty infiltration during 1- (P = 0.007) and 2-year (P < 0.0001) MRI follow-up showed a collagen content of 3.6- and 3.7-fold higher compared to FSHD muscles with no sign of progression. Moreover, the fibrosis was significantly higher in STIR+ muscles who showed a worsening in fatty infiltration in a timeframe of 2 years compared to both STIR− (P = 0.0006) and STIR+ muscles with no sign of progression (P = 0.02). Fibrosis is a sign of muscle degeneration undetectable at MRI never deeply investigated in FSHD patients. Our data show that 23/27 of STIR+ and 12/28 STIR− muscles have a higher amount of collagen deposition compared to healthy muscles. Fibrosis is higher in FSHD muscles with a worsening in fatty infiltration thus suggesting that its evaluation with innovative non-invasive techniques could be a candidate prognostic biomarker for FSHD, to be used to stratify patients and to evaluate the efficacy of therapeutic treatments. [ABSTRACT FROM AUTHOR]

Vitamin D deficiency, prevalent worldwide, is linked to muscle weakness, sarcopenia, and falls. Muscle regeneration is a vital process that allows for skeletal muscle tissue maintenance and repair after injury. PubMed and Web of Science were used to search for studies published prior to May 2023. We assessed eligible studies that discussed the relationship between vitamin D, muscle regeneration in this review. Overall, the literature reports strong associations between vitamin D and skeletal myocyte size, and muscle regeneration. In vitro studies in skeletal muscle cells derived from mice and humans showed vitamin D played a role in regulating myoblast growth, size, and gene expression. Animal studies, primarily in mice, demonstrate vitamin D's positive effects on skeletal muscle function, such as improved grip strength and endurance. These studies encompass vitamin D diet research, genetically modified models, and disease-related mouse models. Relatively few studies looked at muscle function after injury, but these also support a role for vitamin D in muscle recovery. The human studies have also reported that vitamin D deficiency decreases muscle grip strength and gait speed, especially in the elderly population. Finally, human studies reported the benefits of vitamin D supplementation and achieving optimal serum vitamin D levels in muscle recovery after eccentric exercise and surgery. However, there were no benefits in rotator cuff injury studies, suggesting that repair mechanisms for muscle/ligament tears may be less reliant on vitamin D. In summary, vitamin D plays a crucial role in skeletal muscle function, structural integrity, and regeneration, potentially offering therapeutic benefits to patients with musculoskeletal diseases and in post-operative recovery. [ABSTRACT FROM AUTHOR]

The aim was to study the evolution and severity of white striping and wooden breast myopathies and to carry out a study on the parameters of meat quality and allometric growth of male and female broilers at different ages. The experiment was conducted in a broiler house in a completely randomized design, using 960 one-day-old chicks of the Cobb® strain, with 480 chicks of each sex. 96 birds per treatment were slaughtered weekly at the age of 21 to 49 days. The present study analyses the occurrence of myopathies, their scores, and their evolution over the age of the birds, comparing males and females. Further assessments included the allometric coefficient and meat quality analyses such as physical measurements (breast length, width, and thickness), pH, colour (L*, a*, and b*), drip loss, water-holding capacity, cooking loss, and shear force. The results demonstrate that the sex of birds did not affect the occurrence of white striping and wooden breast myopathies. However, the degree of myopathies evolved with advancing age, suggesting the weight as a predisposing factor for these myopathies. The emergence of white striping myopathy occurred as early as in the third week of the birds' life. Wooden breast did not develop as isolated myopathy, occurring only in the concomitant presence of white striping. The allometric coefficient demonstrated that regardless of the sex and age, broiler breast had positive heterogonic growth, i.e. late growth in relation to the other parts of the body.

Abstract Background We examined the association between levothyroxine use and longitudinal MRI biomarkers for thigh muscle mass and composition in at-risk participants for knee osteoarthritis (KOA) and their mediatory role in subsequent KOA incidence. Methods Using the Osteoarthritis Initiative (OAI) data, we included the thighs and corresponding knees of participants at risk but without established radiographic KOA (baseline Kellgren-Lawrence grade (KL) < 2). Levothyroxine users were defined as self-reported use at all annual follow-up visits until the 4th year and were matched with levothyroxine non-users for potential confounders (KOA risk factors, comorbidities, and relevant medications covariates) using 1:2/3 propensity score (PS) matching. Using a previously developed and validated deep learning method for thigh segmentation, we assessed the association between levothyroxine use and 4-year longitudinal changes in muscle mass, including cross-sectional area (CSA) and muscle composition biomarkers including intra-MAT (within-muscle fat), contractile percentage (non-fat muscle CSA/total muscle CSA), and specific force (force per CSA). We further assessed whether levothyroxine use is associated with an 8-year risk of standard KOA radiographic (KL ≥ 2) and symptomatic incidence (incidence of radiographic KOA and pain on most of the days in the past 12 months). Finally, using a mediation analysis, we assessed whether the association between levothyroxine use and KOA incidence is mediated via muscle changes. Results We included 1043 matched thighs/knees (266:777 levothyroxine users:non-users; average ± SD age: 61 ± 9 years, female/male: 4). Levothyroxine use was associated with decreased quadriceps CSAs (mean difference, 95%CI: − 16.06 mm2/year, − 26.70 to − 5.41) but not thigh muscles’ composition (e.g., intra-MAT). Levothyroxine use was also associated with an increased 8-year risk of radiographic (hazard ratio (HR), 95%CI: 1.78, 1.15–2.75) and symptomatic KOA incidence (HR, 95%CI: 1.93, 1.19–3.13). Mediation analysis showed that a decrease in quadriceps mass (i.e., CSA) partially mediated the increased risk of KOA incidence associated with levothyroxine use. Conclusions Our exploratory analyses suggest that levothyroxine use may be associated with loss of quadriceps muscle mass, which may also partially mediate the increased risk of subsequent KOA incidence. Study interpretation should consider underlying thyroid function as a potential confounder or effect modifier. Therefore, future studies are warranted to investigate the underlying thyroid function biomarkers for longitudinal changes in the thigh muscles.

Skeletal muscle is one of the leading frameworks of the musculo-skeletal system, which works in synergy with the bones. Long skeletal muscles provide stability and mobility to the human body and are primarily composed of proteins. Conversely, improper functioning of various skeletal muscles leads to diseases and disorders, namely, age-related muscle disorder called sarcopenia, a group of genetic muscle disorders such as muscular dystrophies, and severe muscle wasting in cancer known as cachexia. However, skeletal muscle has an excellent ability to undergo hypertrophy and enhanced functioning during sustained exercise over time. Indeed, these processes of skeletal muscle regeneration/hypertrophy, as well as degeneration and atrophy, involve an interplay of various signaling pathways. Myostatin is one such chemokine/myokine with a significant contribution to muscle regeneration or atrophy in multiple conditions. In this review, we try to put together the role and regulation of myostatin as a function of muscle regeneration extrapolated to multiple aspects of its molecular functions.

Abstract Background Cathelicidin, an antimicrobial peptide, plays a key role in regulating bacterial killing and innate immunity; however, its role in skeletal muscle function is unknown. We investigated the potential role of cathelicidin in skeletal muscle pathology resulting from acute injury and Duchenne muscular dystrophy (DMD) in mice. Methods Expression changes and muscular localization of mouse cathelicidin‐related antimicrobial peptide (Cramp) were examined in the skeletal muscle of normal mice treated with chemicals (cardiotoxin and BaCl2) or in dystrophic muscle of DMD mouse models (mdx, mdx/Utrn+/− and mdx/Utrn−/−). Cramp penetration into myofibres and effects on muscle damage were studied by treating synthetic peptides to mouse skeletal muscles or C2C12 myotubes. Cramp knockout (KO) mice and mdx/Utrn/Cramp KO lines were used to determine whether Cramp mediates muscle degeneration. Muscle pathophysiology was assessed by histological methods, serum analysis, grip strength and lifespan. Molecular factors targeted by Cramp were identified by the pull‐down assay and proteomic analysis. Results In response to acute muscle injury, Cramp was activated in muscle‐infiltrating neutrophils and internalized into myofibres. Cramp treatments of mouse skeletal muscles or C2C12 myotubes resulted in muscle degeneration and myotube damage, respectively. Genetic ablation of Cramp reduced neutrophil infiltration and ameliorated muscle pathology, such as fibre size (P

Purpose: We investigated loco-regional degenerative changes' association with incidentally found non-traumatic vertebral body fractures of the lower thoracic and lumbar spine in older patients. Methods: The patient collective included patients in the age range of 50 to 90 years. Vertebral bodies from T7 to L5 were included. Vertebral body fractures were classified according to Genant. The following loco-regional osseous and extra-osseous degenerative changes were included: osteochondrosis, spondylarthritis, facet joint asymmetries, spondylolisthesis, scoliosis as well as fatty degeneration and asymmetry of the autochthonous back muscles. Patients with traumatic and tumor-related vertebral body fractures were excluded. Non-traumatic fractures of the lower thoracic and lumbar spine were evaluated separately. The Mann–Whitney U-test was used, and relative risks (RRs) were calculated for statistics. Pearson's correlations (Rs) were used to correlate grades of degenerative changes and fracture severities. Results: 105 patients were included. Fatty deposits in the autochthonous muscles of the lower thoracic and the lumbar spine were associated with non-traumatic vertebral body fractures in the lower thoracic spine (p = 0.005, RR = 4.92). In contrast, muscle fatness of the autochthonous muscles was not a risk factor for lumbar spine fractures (p = 0.157, RR = 2.04). Additionally, we found a moderate correlation between fatty degeneration of the autochthonous muscles and the severity of fractures in the lower thoracic spine (RR = 0.34, p < 0.001). The other degenerative changes did not present any significant difference or correlation between the evaluated groups. Conclusions: Fatty degeneration of the autochthonous spinal musculature is associated with incidentally found non-traumatic fractures of the lower thoracic spine. [ABSTRACT FROM AUTHOR]

The aim was to study the evolution and severity of white striping and wooden breast myopathies and to carry out a study on the parameters of meat quality and allometric growth of male and female broilers at different ages. The experiment was conducted in a broiler house in a completely randomized design, using 960 one-day-old chicks of the Cobb® strain, with 480 chicks of each sex. 96 birds per treatment were slaughtered weekly at the age of 21 to 49 days. The present study analyses the occurrence of myopathies, their scores, and their evolution over the age of the birds, comparing males and females. Further assessments included the allometric coefficient and meat quality analyses such as physical measurements (breast length, width, and thickness), pH, colour (L*, a*, and b*), drip loss, water-holding capacity, cooking loss, and shear force. The results demonstrate that the sex of birds did not affect the occurrence of white striping and wooden breast myopathies. However, the degree of myopathies evolved with advancing age, suggesting the weight as a predisposing factor for these myopathies. The emergence of white striping myopathy occurred as early as in the third week of the birds' life. Wooden breast did not develop as isolated myopathy, occurring only in the concomitant presence of white striping. The allometric coefficient demonstrated that regardless of the sex and age, broiler breast had positive heterogonic growth, i.e. late growth in relation to the other parts of the body. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a disease of joint degeneration and impaired function. Muscle atrophy, fatty infiltration, and fibrosis are degenerative features of muscle injury and predict poor outcomes in some degenerative and exercise-related injuries. Patients with glenohumeral joint OA usually have rotator cuff muscle degeneration, even though the rotator cuff is intact. However, the mechanism and correlation between OA and degeneration of muscles around joints are still unknown. Forty-five 12-month-old C57BL/6J mice received a single injection of monoiodoacetic acid into the right glenohumeral joint. The sham group was injected with saline on the same day in the right glenohumeral joint. Three and 6 weeks after the operation, gait analysis was conducted to evaluate the function of the forelimb. Then, the shoulder joint and supraspinatus muscle were collected for histologic staining, reverse transcription quantitative polymerase chain reaction, and biomechanics test. Correlations between fat area fraction in muscle, percentage wet muscle weight change or Osteoarthritis Research Society International score, and gait analysis/muscle mechanics tests were assessed using Pearson's correlation coefficient or Spearman's correlation coefficient. Compared with the sham group, the monoiodoacetic acid group developed significant glenohumeral joint OA and the supraspinatus muscle developed significant fatty infiltration and muscle atrophy. Shoulder function correlated with glenohumeral joint OA/rotator cuff muscle severity, weight loss, and fatty infiltration. In mice, glenohumeral joint OA can lead to rotator cuff degeneration and inferior limb function. The small animal model could be a powerful tool to further study the potential mechanisms between glenohumeral OA and rotator cuff muscle degeneration. [ABSTRACT FROM AUTHOR]

Abstract Background To compare changes in the composition of paraspinal muscles of patients with ankylosing spondylitis (AS) and matched healthy controls using T2 mapping and T2 IDEAL and correlate the quantitative magnetic resonance imaging (qMRI) results with clinical assessments of AS patients. Method In total, 37 AS patients and 37 healthy controls were enrolled in the case control study. T2 mapping with and without fat saturation and IDEAL imaging were used to assess the multifidus (MF) and erector spinae (ES) at the levels of L3/L4 and L4/L5 for all subjects. Mean T2non-fatsat, T2fat, T2fatsat, cross-sectional area (CSA), and fat fraction (FF) were compared between AS and healthy controls. Correlations of qMRI results with clinical assessments were analyzed in AS. Results Significantly elevated mean T2non-fatsat values and the FF of the MF and ES at both levels were observed in AS and compared to the controls (p 0.05). Conclusions Our findings indicate that using a combination of IDEAL and T2 mapping may provide deeper insights into the pathophysiological degeneration of paraspinal muscles in AS.

Skeletal muscle is the most abundant tissue in the body and requires high levels of energy to function properly. Skeletal muscle allows voluntary movement and body posture, which require different types of fiber, innervation, energy, and metabolism. Here, we summarize the contribution received at the time of publication of this Introductory Issue for the Special Issue dedicated to "Skeletal Muscle Atrophy: Mechanisms at a Cellular Level". The Special Issue is divided into three sections. The first is dedicated to skeletal muscle pathophysiology, the second to disease mechanisms, and the third to therapeutic development. [ABSTRACT FROM AUTHOR]

Muscular dystrophies (DM) are neurological conditions of great complexity and severity that involve progressive loss of muscle mass and associated reduction in muscle strength. The causes are genetic and involve mutations in the dystrophin gene that lead to the absence or deficiency of functional dystrophin, a cytoskeletal protein that enables general muscle function. In neuromuscular dystrophies there are direct molecular mechanisms responsible for exercise intolerance and inability to contract muscles. The use of therapeutic physical exercises is a way to slow down the preogression of the disease, to combat the loss of functionality of the muscle fibers as well as to delay the appearance of secondary manifestations of the disease, manifestations that occur with the ability to ambulate and with the installation of sedentarism caused by muscle weakness and degeneration. The effects of therapeutic exercise on patients with muscular dystrophy (including the effects of exceptional or maximal exercise) have been analyzed in the literature, and it has been found that aerobic exercise performed under the guidance of a physical therapist can be effective in improving oxidative capacity and progressive muscle function of the patient. The exercises must be adapted to the individual case, depending on the patient's general condition and availability of effort. Careful supervision and monitoring of patients can achieve the objectives obtained in the form of beneficial effects for the affected muscles. The present dissemination proposes a brief presentation of different types of therapeutic exercises (aerobic, endurance, resistance) and their role in the recovery program of patients with progressive muscular dystrophies. [ABSTRACT FROM AUTHOR]

Per- and polyfluoroalkyl substances (PFASs), including perfluorooctane sulfonate (PFOS) and its alternative 6:2 chlorinated polyfluoroalkyl ether sulfonate (F53B), are widely used in industries, leading to their presence in aquatic environments and potential adverse effects on marine organisms, particularly during early development. This study investigates the effects of PFOS and F53B on larval development and metamorphosis in Mytilus coruscus. Exposure to 4.7 and 39.2 μg/L PFOS and 1.2, 7.5, and 91.8 μg/L F53B significantly reduced larval metamorphosis compared to controls. PFOS and F53B exposure disrupted the normal degeneration of the larval velum and velum retractor muscles, essential for metamorphosis. Lower concentrations (1.2 and 7.5 μg/L) of F53B had a stronger inhibitory effect than 91.8 μg/L, suggesting F53B may act as an endocrine disruptor. Transcriptomic analysis revealed 801 differentially expressed genes in PFOS-exposed larvae and 2496 DEGs in F53B-exposed larvae, affecting pathways related to neural communication, cellular processes, and developmental signaling (e.g., Hedgehog, PI3K-AKT, Hippo, and MAPK). Real-time quantitative polymerase chain reaction confirmed the down-regulation of genes related to growth and development in both treatment groups, indicating suppressed growth and development. Our findings suggest that PFOS and F53B impacted larval metamorphosis and potentially altered the developmental trajectories of M. coruscus under environmental contamination scenarios. This study highlights the significant ecological implications of PFOS and F53B exposure on marine bivalve development, demonstrating their capacity to disrupt larval metamorphosis, thereby underscoring the potential risks these persistent pollutants pose to marine ecosystems and the early life stages of aquatic organisms., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025 Elsevier B.V. All rights reserved.)

Muscle degeneration is a common issue caused by rotator cuff tear (RCT) which significantly affects prognosis. Muscle stem cells (MuSCs) play a crucial role to prevent muscle degeneration after RCT. However, the pathological changes and detailed molecular mechanism underlying the myogenesis of MuSCs after RCT remain incomplete. The current study established single-cell landscape of supraspinatus muscles and found decreased expression of PIEZO1 and impaired myogenic potential of MuSCs from RCT patients. Reduced expression of PIEZO1 impaired the myogenesis of MuSCs by inhibiting the ERK/MAPK pathways. Furthermore, selective PIEZO1 agonist Yoda1 had the potential to alleviate muscle degeneration and improve shoulder function following RCT. This study emphasized the role of PIEZO1 in the myogenesis of MuSCs and suggested that activating PIEZO1 could be a potential non-surgical treatment option to reduce muscle degeneration after RCT., Competing Interests: The authors have declared no conflict of interest., (© 2024 The Author(s).)

Abstract Background Degeneration of shoulder muscle tissues often result in tearing, causing pain, disability and loss of independence. Differential muscle involvement patterns have been reported in tears of shoulder muscles, yet the molecules involved in this pathology are poorly understood. The spatial distribution of biomolecules across the affected tissue can be accurately obtained with matrix‐assisted laser desorption/ionization mass spectrometry imaging (MALDI‐MSI). The goal of this pilot study was to decipher the metabolic landscape across shoulder muscle tissues and to identify signatures of degenerated muscles in chronic conditions. Methods Paired biopsies of two rotator cuff muscles, torn infraspinatus and intact teres minor, together with an intact shoulder muscle, the deltoid, were collected during an open tendon transfer surgery. Five patients, average age 65.2 ± 3.8 years, were selected for spatial metabolic profiling using high‐spatial resolution (MALDI‐TOF) and high‐mass resolution (MALDI‐FTICR) MSI in negative or positive ion mode. Metabolic signatures were identified using data‐driven analysis. Verifications of spatial localization for selected metabolic signatures were carried out using antibody immunohistology. Results Data‐driven analysis revealed major metabolic differences between intact and degenerated regions across all muscles. The area of degenerated regions, encompassed of fat, inflammation and fibrosis, significantly increased in both rotator cuff muscles, teres minor (27.9%) and infraspinatus (22.8%), compared with the deltoid (8.7%). The intact regions were characterized by 49 features, among which lipids were recognized. Several of the identified lipids were specifically enriched in certain myofiber types. Degenerated regions were specifically marked by the presence of 37 features. Heme was the most abundant metabolite in degenerated regions, whereas Heme oxygenase‐1 (HO‐1), which catabolizes heme, was found in intact regions. Higher HO‐1 levels correlated with lower heme accumulation. Conclusions Degenerated regions are distinguished from intact regions by their metabolome profile. A muscle‐specific metabolome profile was not identified. The area of tissue degeneration significantly differs between the three examined muscles. Higher HO‐1 levels in intact regions concurred with lower heme levels in degenerated regions. Moreover, HO‐1 levels discriminated between dysfunctional and functional rotator cuff muscles. Additionally, the enrichment of specific lipids in certain myofiber types suggests that lipid metabolism differs between myofiber types. The signature metabolites can open options to develop personalized treatments for chronic shoulder muscles degeneration.

Background and Objectives: The aim of this study was to evaluate the impact of sagittal imbalance based on pelvic incidence–lumbar lordosis (PI-LL) mismatch on the analgesic efficacy of epidural steroid injection in geriatric patients. Materials and Methods: Patients aged 65 years or older who received lumbar epidural steroid injections under fluoroscopy were enrolled. The cutoff of PI-LL mismatch >20° was used as an indicator of a marked sagittal imbalance. The cross-sectional area of the psoas and paraspinal muscles, as well as the paraspinal fat infiltration grade were measured. A 50% or more decrease in pain score at four weeks after injection was considered as good analgesia. Variables were compared between PI-LL ≤ 20° and >20° groups and multivariate analysis was used to identify factors related to pain relief after injection. Results: A total of 237 patients consisting of 150 and 87 patients in the PI-LL ≤ 20° and >20° groups, respectively, were finally analyzed. Female patients, patients with lumbar surgery history, and the smaller cross-sectional area of the psoas muscles were predominantly observed in patients with sagittal imbalance. There was no difference in analgesic outcome after injection according to the PI-LL mismatch (good analgesia 60.0 vs. 60.9%, p = 0.889). Multivariate analysis showed that pre-injection opioid use, moderate to severe foraminal stenosis, and high-graded paraspinal fat infiltration were significantly associated with poor analgesia after injection. Conclusions: There was no significant correlation between sagittal spinopelvic alignment and pain relief after lumbar epidural steroid injection for geriatric patients. [ABSTRACT FROM AUTHOR]

Massive rotator cuff tears (MRCTs) of the shoulder cause disability and pain among the adult population. In chronic injuries, the tendon retraction and subsequently the loss of mechanical load lead to muscle atrophy, fat accumulation, and fibrosis formation over time. The intrinsic repair mechanism of muscle and the successful repair of the torn tendon cannot reverse the muscle degeneration following MRCTs. To address these limitations, we developed an electroconductive matrix by incorporating graphene nanoplatelets (GnPs) into aligned poly(l-lactic acid) (PLLA) nanofibers. This study aimed to understand 1) the effects of GnP matrices on muscle regeneration and inhibition of fat formation in vitro and 2) the ability of GnP matrices to reverse muscle degenerative changes in vivo following an MRCT. The GnP matrix significantly increased myotube formation, which can be attributed to enhanced intracellular calcium ions in myoblasts. Moreover, the GnP matrix suppressed adipogenesis in adipose-derived stem cells. These results supported the clinical effects of the GnP matrix on reducing fat accumulation and muscle atrophy. The histological evaluation showed the potential of the GnP matrix to reverse muscle atrophy, fat accumulation, and fibrosis in both supraspinatus and infraspinatus muscles at 24 and 32 wk after the chronic MRCTs of the rat shoulder. The pathological evaluation of internal organs confirmed the long-term biocompatibility of the GnP matrix. We found that reversing muscle degenerative changes improved the morphology and tensile properties of the tendon compared with current surgical techniques. The long-term biocompatibility and the ability of the GnP matrix to treat muscle degeneration are promising for the realization of MRCT healing and regeneration. [ABSTRACT FROM AUTHOR]

Background: To compare changes in the composition of paraspinal muscles of patients with ankylosing spondylitis (AS) and matched healthy controls using T2 mapping and T2 IDEAL and correlate the quantitative magnetic resonance imaging (qMRI) results with clinical assessments of AS patients.Method: In total, 37 AS patients and 37 healthy controls were enrolled in the case control study. T2 mapping with and without fat saturation and IDEAL imaging were used to assess the multifidus (MF) and erector spinae (ES) at the levels of L3/L4 and L4/L5 for all subjects. Mean T2non-fatsat, T2fat, T2fatsat, cross-sectional area (CSA), and fat fraction (FF) were compared between AS and healthy controls. Correlations of qMRI results with clinical assessments were analyzed in AS.Results: Significantly elevated mean T2non-fatsat values and the FF of the MF and ES at both levels were observed in AS and compared to the controls (p < 0.05). The mean T2fatsat values of ES and MF were significantly higher only at the level of L3/L4 in AS compared to healthy controls (p < 0.05). A loss of muscle CSA compatible with atrophy was present in MF and ES at both levels in AS compared to the controls (p < 0.05). Weak to moderate positive correlations were found between FF and age and disease duration in AS (r = 0.318-0.415, p < 0.05). However, such positive correlation was not observed between FF and disease duration after adjusting for age (p > 0.05).Conclusions: Our findings indicate that using a combination of IDEAL and T2 mapping may provide deeper insights into the pathophysiological degeneration of paraspinal muscles in AS. [ABSTRACT FROM AUTHOR]

Background: Monitoring the fatty infiltration (FI) process in rotator cuff muscles is of value in establishing a treatment plan and predicting the postoperative prognosis. Quantitative T1 mapping shows promise for evaluating muscle degeneration, while its validity in monitoring rotator cuff muscle FI progression needs further investigation. Purpose: To determine the validity of T1 mapping in monitoring FI progression of rotator cuff muscles. Study Design: Controlled laboratory study. Methods: Sprague-Dawley rats (N = 108) underwent left supraspinatus (SS) and infraspinatus (IS) tenotomy only (TT), suprascapular nerve transection only (NT), or SS and IS tenotomy plus suprascapular nerve transection (TT+NT). Sham surgery on the right shoulder served as the control. The magnetic resonance imaging examination included T1 mapping performed at 12, 16, and 20 weeks postoperation. SS and IS muscles were harvested to quantitatively evaluate FI via direct evaluation (triglyceride quantification assay and histological analysis) at the same predetermined intervals. The correlation of the imaging data with direct evaluation of rotator cuff muscles was analyzed. Results: T1 values were significantly lower in left SS and IS muscles at 12, 16, and 20 weeks postoperation as compared with those on the right side. T1 values of the left SS and IS muscles were continuously decreased in all groups. The TT+NT group had a greater decrease in T1 value than did the TT and NT groups. Triglyceride quantification assay and histological analysis demonstrated significant and progressive FI of the left SS and IS muscles in the 3 groups. The most serious FI changes were observed in the TT+NT group. T1 values were also well correlated with triglyceride contents and area fractions of fat. Conclusion: T1 mapping can be an effective imaging modality for sensitive and quantitative monitoring of FI progression in rotator cuff muscles. Clinical Relevance: The findings of this study provide a tool for researchers to noninvasively and quantitatively monitor the process of muscle degeneration, contributing to the evaluation of surgical indication and postoperative prognosis. [ABSTRACT FROM AUTHOR]

The rabbit supraspinatus is a useful translational model for rotator cuff (RC) repair because it recapitulates muscle atrophy and fat accumulation observed in humans after a chronic tear (the "first hit"). However, a timeline of RC tissue response after repair, especially with regard to recent evidence of muscle degeneration and lack of regeneration, is currently unavailable. Thus, the purpose of this study was to characterize the progression of muscle and fat changes over time after the repair of a chronic RC tear in the rabbit model. Two rounds of experiments were conducted in 2017–2018 and 2019–2020 with N = 18 and 16 skeletally mature New Zealand White rabbits, respectively. Animals underwent left supraspinatus tenotomy with repair 8 weeks later. The unoperated right shoulder served as control. The rabbits were sacrificed at 1-, 2-, 4-, and 8-weeks post-repair for histological and biochemical analysis. Atrophy, measured by fiber cross-sectional area and muscle mass, was greatest around 2 weeks after repair. Active muscle degeneration peaked at the same time, involving 8% of slide areas. There was no significant regeneration at any timepoint. Fat accumulation and fibrosis were significantly increased across all time points compared to contralateral. Statement of Clinical Significance: These results demonstrate model reproducibility and a "second hit" phenomenon of repair-induced muscle atrophy and degeneration which partially recovers after a short time, while increased fat and fibrosis persist. [ABSTRACT FROM AUTHOR]

The rabbit supraspinatus is a useful translational model for rotator cuff (RC) repair because it recapitulates muscle atrophy and fat accumulation observed in humans after a chronic tear (the “first hit”). However, a timeline of RC tissue response after repair, especially with regard to recent evidence of muscle degeneration and lack of regeneration, is currently unavailable. Thus, the purpose of this study was to characterize the progression of muscle and fat changes over time after the repair of a chronic RC tear in the rabbit model. Two rounds of experiments were conducted in 2017–2018 and 2019–2020 with N = 18 and 16 skeletally mature New Zealand White rabbits, respectively. Animals underwent left supraspinatus tenotomy with repair 8 weeks later. The unoperated right shoulder served as control. The rabbits were sacrificed at 1-, 2-, 4-, and 8-weeks post-repair for histological and biochemical analysis. Atrophy, measured by fiber cross-sectional area and muscle mass, was greatest around 2 weeks after repair. Active muscle degeneration peaked at the same time, involving 8% of slide areas. There was no significant regeneration at any timepoint. Fat accumulation and fibrosis were significantly increased across all time points compared to contralateral. Statement of Clinical Significance: These results demonstrate model reproducibility and a “second hit” phenomenon of repair-induced muscle atrophy and degeneration which partially recovers after a short time, while increased fat and fibrosis persist.

Acute localized irradiation accidents may evolve into a musculocutaneous radiation-induced syndrome that leaves a significant underlying muscle defect despite standard treatment. The identification of new therapeutic targets is, therefore, necessary to improve post-irradiation muscle repair. Thus, the validation of an in vivo model of radiation-induced muscle injury has been initiated in C57Bl/6J mice. In the model presented in this study, the high-dose ionizing radiation exposure is focused on gastrocnemius and soleus muscles, does not affect bones, and is a part of hindlimb vascularization. It aims at identifying original metabolic pathways specifically involved in muscle damage and evaluating innovative therapeutic strategies.

Several scientific evidence have shown that exposure to microgravity has a significant impact on the health of the musculoskeletal system by altering the expression of proteins and molecules involved in bone–muscle crosstalk, which is also observed in the research of microgravity effect simulation. Among these, the expression pattern of myostatin appears to play a key role in both load-free muscle damage and the progression of age-related musculoskeletal disorders, such as osteoporosis and sarcopenia. Based on this evidence, we here investigated the efficacy of treatment with anti-myostatin (anti-MSTN) antibodies on primary cultures of human satellite cells exposed to 72 h of random positioning machine (RPM). Cell cultures were obtained from muscle biopsies taken from a total of 30 patients (controls, osteoarthritic, and osteoporotic) during hip arthroplasty. The Pax7 expression by immunofluorescence was carried out for the characterization of satellite cells. We then performed morphological evaluation by light microscopy and immunocytochemical analysis to assess myostatin expression. Our results showed that prolonged RPM exposure not only caused satellite cell death, but also induced changes in myostatin expression levels with group-dependent variations. Surprisingly, we observed that the use of anti-MSTN antibodies induced a significant increase in cell survival after RPM exposure under all experimental conditions. Noteworthy, we found that the negative effect of RPM exposure was counteracted by treatment with anti-MSTN antibodies, which allowed the formation of numerous myotubes. Our results highlight the role of myostatin as a major effector of the cellular degeneration observed with RPM exposure, suggesting it as a potential therapeutic target to slow the muscle mass loss that occurs in the absence of loading.

Several scientific evidence have shown that exposure to microgravity has a significant impact on the health of the musculoskeletal system by altering the expression of proteins and molecules involved in bone–muscle crosstalk, which is also observed in the research of microgravity effect simulation. Among these, the expression pattern of myostatin appears to play a key role in both load-free muscle damage and the progression of age-related musculoskeletal disorders, such as osteoporosis and sarcopenia. Based on this evidence, we here investigated the efficacy of treatment with anti-myostatin (anti-MSTN) antibodies on primary cultures of human satellite cells exposed to 72 h of random positioning machine (RPM). Cell cultures were obtained from muscle biopsies taken from a total of 30 patients (controls, osteoarthritic, and osteoporotic) during hip arthroplasty. The Pax7 expression by immunofluorescence was carried out for the characterization of satellite cells. We then performed morphological evaluation by light microscopy and immunocytochemical analysis to assess myostatin expression. Our results showed that prolonged RPM exposure not only caused satellite cell death, but also induced changes in myostatin expression levels with group-dependent variations. Surprisingly, we observed that the use of anti-MSTN antibodies induced a significant increase in cell survival after RPM exposure under all experimental conditions. Noteworthy, we found that the negative effect of RPM exposure was counteracted by treatment with anti-MSTN antibodies, which allowed the formation of numerous myotubes. Our results highlight the role of myostatin as a major effector of the cellular degeneration observed with RPM exposure, suggesting it as a potential therapeutic target to slow the muscle mass loss that occurs in the absence of loading. [ABSTRACT FROM AUTHOR]

Background and Objectives: The aim of this study was to evaluate the impact of sagittal imbalance based on pelvic incidence–lumbar lordosis (PI-LL) mismatch on the analgesic efficacy of epidural steroid injection in geriatric patients. Materials and Methods: Patients aged 65 years or older who received lumbar epidural steroid injections under fluoroscopy were enrolled. The cutoff of PI-LL mismatch >20° was used as an indicator of a marked sagittal imbalance. The cross-sectional area of the psoas and paraspinal muscles, as well as the paraspinal fat infiltration grade were measured. A 50% or more decrease in pain score at four weeks after injection was considered as good analgesia. Variables were compared between PI-LL ≤ 20° and >20° groups and multivariate analysis was used to identify factors related to pain relief after injection. Results: A total of 237 patients consisting of 150 and 87 patients in the PI-LL ≤ 20° and >20° groups, respectively, were finally analyzed. Female patients, patients with lumbar surgery history, and the smaller cross-sectional area of the psoas muscles were predominantly observed in patients with sagittal imbalance. There was no difference in analgesic outcome after injection according to the PI-LL mismatch (good analgesia 60.0 vs. 60.9%, p = 0.889). Multivariate analysis showed that pre-injection opioid use, moderate to severe foraminal stenosis, and high-graded paraspinal fat infiltration were significantly associated with poor analgesia after injection. Conclusions: There was no significant correlation between sagittal spinopelvic alignment and pain relief after lumbar epidural steroid injection for geriatric patients.

A recessive X-linked illness called Duchenne muscular dystrophy (DMD) is characterized by increasing muscle weakening and degradation. It primarily affects boys and is one of the most prevalent and severe forms of muscular dystrophy. Mutations in the DMD gene, which codes for the essential protein dystrophin, which aids in maintaining the stability of muscle cell membranes during contraction, are the cause of the illness. Dystrophin deficiency or malfunction damages muscle cells, resulting in persistent inflammation and progressive loss of muscular mass. The pathophysiology and genetic foundation of DMD are thoroughly examined in this review paper, focusing on the function of the NF-κB signaling system in the disease's progression. An important immune response regulator, NF-κB, is aberrantly activated in DMD, which exacerbates the inflammatory milieu in dystrophic muscles. Muscle injury and fibrosis are exacerbated and muscle regeneration is hampered by the pro-inflammatory cytokines and chemokines that are produced when NF-κB is persistently activated in muscle cells. The paper also examines our existing knowledge of treatment approaches meant to inhibit the progression of disease by modifying NF-κB signaling. These include new molecular techniques, gene treatments, and pharmacological inhibitors that are intended to lessen inflammation and improve muscle healing. Furthermore covered in the analysis is the significance of supportive care for DMD patients, including physical therapy and corticosteroid treatment, in symptom management and quality of life enhancement. The article seeks to provide a thorough understanding of the mechanisms causing DMD, possible therapeutic targets, and developing treatment options by combining recent research findings. This will provide clinicians and researchers involved in DMD care and research with invaluable insights., Competing Interests: Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, R et al.)

The muscle is the principal tissue that is capable to transform potential energy into kinetic energy. This process is due to the transformation of chemical energy into mechanical energy to enhance the movements and all the daily activities. However, muscular tissues can be affected by some pathologies associated with genetic alterations that affect the expression of proteins. As the muscle is a highly organized structure in which most of the signaling pathways and proteins are related to one another, pathologies may overlap. Duchenne muscular dystrophy (DMD) is one of the most severe muscle pathologies triggering degeneration and muscle necrosis. Several mathematical models have been developed to predict muscle response to different scenarios and pathologies. The aim of this review is to describe DMD and Becker muscular dystrophy in terms of cellular behavior and molecular disorders and to present an overview of the computational models implemented to understand muscle behavior with the aim of improving regenerative therapy., (© 2024 Wiley Periodicals LLC.)

Introduction: Skeletal muscle degeneration is a common effect of chronic muscle injuries, including fibrosis and fatty infiltration, which is the replacement of preexisting parenchymal tissue by extracellular matrix proteins and abnormal invasive growth of fibroblasts and adipocytes., Method: This remodeling limits muscle function and strength, eventually leading to reduced quality of life for those affected. Chemokines play a major role in the regulation of immunocyte migration, inflammation, and tissue remodeling and are implicated in various fibrotic and degenerative diseases. In this study, we aimed to investigate the role of the B-cell chemokine CXCL13 in the gastrocnemius muscle of the Achilles tendon rupture model mouse. We hypothesize that CXCL13 may promote fibrosis and aggravate skeletal muscle degeneration. We performed RNA sequencing and bioinformatics analysis of gastrocnemius muscle from normal and model mice to identify differentially expressed genes and signal pathways related to skeletal muscle degeneration and fibrosis., Results: Our results show that CXCL13 is highly expressed in chronically degenerating skeletal muscle. Furthermore, CXCL13-neutralising antibodies with therapeutic potential were observed to inhibit fibrosis and adipogenesis in vivo and in vitro., Conclusion: Our study reveals the underlying therapeutic implications of CXCL13 inhibition for clinical intervention in skeletal muscle degeneration, thereby improving patient prognosis., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Glossectomy is a surgical procedure performed to remove all or part of the tongue in patients with cancer. The removal of a significant part of the tongue has a marked effect on speech and swallowing function, as patients may lose not only the tongue muscles but also the median lingual septum (MLS). Therefore, to achieve successful tongue regeneration, it is necessary to investigate the developmental processes of not only the tongue muscles but also the MLS. This study was conducted to clarify the mutual development of the tongue muscles and the MLS in human fetuses. Serial or semi-serial histological sections from 37 embryos and fetuses (aged 5-39 weeks) as well as nine adults were analyzed. The MLS appeared at Carnegie stage 15 (CS15), and until 12 weeks of gestation, abundant fibers of the intrinsic transverse muscle crossed the septum in the entire tongue. However, in near-term fetuses and adults, the contralaterally extending muscles were restricted to the deepest layer just above the genioglossus muscle. This finding indicates that the crossing transverse muscle showed the highest density at mid-term. A thorough understanding of both the MLS and the tongue muscles is necessary for successful tongue regeneration., (© 2023 American Association for Anatomy.)

A decline in muscle strength is a key factor responsible for physical dysfunction in older individuals. Both loss of muscle quantity and quality are associated with muscle strength decline. While the gold standard method for evaluating muscle mass and quality is magnetic resonance imaging, it is not suitable for clinical settings because of the measurement and analysis costs. Bioelectrical impedance analysis (BIA) and B-mode ultrasonography are clinically useful alternatives for skeletal muscle assessment owing to their feasibility and noninvasiveness. The recent advancements in the techniques for BIA and ultrasonography have improved their accuracy in assessing skeletal muscle quantity and quality, making them useful in detecting age-related and disease-specific alterations. This review comprehensively analyzes the advantages of using BIA and ultrasound imaging for assessing skeletal muscle quantity and quality and detecting muscle degeneration. We summarize the recent findings regarding age-related changes in muscle characteristics and the associations of muscle degeneration with physical dysfunction in patients with knee osteoarthritis. Furthermore, we discuss the clinical application of skeletal muscle assessment using BIA and ultrasound for evaluating training effects and exercise prescription., Competing Interests: The author declares no conflicts of interest., (©2024 Japanese Society of Physical Therapy.)

Toxicity caused by chronic hyperglycemia is a significant factor affecting skeletal muscle myogenesis, resulting in diabetic myopathy. Chronic and persistent hyperglycemia causes activation of the atrophy-related pathways in the skeletal muscles, which eventually results in inflammation and muscle degeneration. To counteract this process, various bioactive compound has been studied for their reversal or hypertrophic effect. In this study, we explored the molecular mechanisms associated with reversing glucotoxicity's effect in C2C12 cells by arachidonic acid (AA). We found a substantial increase in the pro-inflammatory cytokines and ROS production in hyperglycemic conditions, mitigated by AA supplementation. We found that AA supplementation restored protein synthesis that was downregulated under glucotoxicity conditions. AA enhanced myogenesis by suppressing high glucose induced inflammation and ROS production and enhancing protein synthesis. These results imply that AA has cytoprotective actions against hyperglycemia-induced cytotoxicity. [Display omitted] [ABSTRACT FROM AUTHOR]

Crustacean hemocytes are important mediators of immune functions such as coagulation and phagocytosis. We employed an in situ approach to investigate the ultrastructural behavior of hemocytes during coagulation and phagocytosis in the early stages after injury caused by leg amputation, using transmission electron microscopy technique in marbled crayfish Procambarus virginalis. Hemocytes underwent drastic morphological changes during coagulation. The morphology of the cytoplasmic granules changed from electron-dense to electron-lucent forms in an expanding manner. The transformed granules containing amorphous electron-lucent material were observed to merge and discharge their contents into extracellular space for coagulation. We also observed that the contents of the nucleus participate in the process of coagulation. In addition, leg amputation induced extensive muscle degeneration and necrotic tissues were avidly taken up by the phagocytic hemocytes containing distinct phagosomes. Interestingly, we observed for the first time how the digested contents of phagocytized necrotic tissues are incorporated into granules and other cellular components that change the cell morphology by increasing the granularity of the hemocytes. Nevertheless, the degranulation of hemocytes during coagulation can also reduce their granularity. Given that morphological traits are important criteria for hemocyte classification, these morphological changes that occur during coagulation and phagocytosis must be taken into account. • Coagulation and phagocytosis extensively change the morphology of hemocytes. • During degranulation, electron-dense granules expand and transform into electron-lucent forms. • The contents of the hemocyte nucleus participate in coagulation. • Phagocytic hemocytes ingest and incorporate degenerated muscles that affect their granularity. [ABSTRACT FROM AUTHOR]

Liquid biopsy provides a promising alternative for the detection of disease-specific markers due to its superior noninvasive and original tissue representativeness. Liquid biopsies have a wide range of health and disease applications involving components ranging from circulating cells to acellular nucleic acid molecules and other metabolites. Here, we review the different components of liquid biopsy and investigate the most advanced noninvasive methods for detecting these components as well as their existing problems and trends. In particular, we emphasize the importance of analyzing liquid biopsy data from extracellular vesicles and small nucleic acids in neurological and muscle degeneration, with the aim of using this technique to enhance personalized healthcare. Although previous reviews have focused on cancer, this review mainly emphasizes the potential application of extracellular vesicles and microRNAs in liquid biopsy in neurodegeneration and muscle degeneration., (© 2023. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

BACKGROUND. After rotator cuff tear, properties of the torn muscle predict failed surgical repair. OBJECTIVE. The purpose of our study was to explore the utility of preoperative shear-wave elastography (SWE) measurements of the supraspinatus muscle to predict successful rotator cuff repair, including comparison with MRI-based measures. METHODS. This prospective study included 74 patients (37 men, 37 women; mean age, 63.9 ± 10.0 [SD] years) who underwent rotator cuff repair between May 2019 and January 2021. Patients underwent preoperative clinical shoulder MRI and investigational shoulder ultrasound including SWE using shear modulus. The mean elasticity values of the supraspinatus and trapezius muscles were measured, and the elasticity ratio (i.e., ratio of mean elasticity of supraspinatus muscle to mean elasticity of trapezius muscle) was calculated. The muscular fatty infiltration score (1-3 scale) was recorded on gray-scale ultrasound. On MRI, muscular fatty infiltration was assessed by Goutallier grade (0-4 scale), and muscular atrophy was assessed by the occupation ratio (ratio of cross-sectional areas of supraspinatus muscle and supraspinatus fossa) and by the muscle atrophy grade (0-3 scale). After rotator cuff repair, the surgeon classified procedures as achieving sufficient ( n = 60) or insufficient ( n = 14) repair. RESULTS. Patients with insufficient repair, versus those with sufficient repair, more commonly exhibited a large (3-5 cm) tear (100.0% vs 50.0%). Patients with insufficient, versus sufficient, repair exhibited higher mean Goutallier grade (3.8 ± 0.4 vs 1.9 ± 1.1), mean muscle atrophy grade (2.0 ± 0.8 vs 0.5 ± 0.7), mean supraspinatus elasticity (44.15 ± 8.06 vs 30.84 ± 7.89 kPa), mean elasticity ratio (3.66 ± 0.66 vs 1.83 ± 0.58), and mean gray-scale fatty infiltration grade (2.86 ± 0.36 vs 1.63 ± 0.66) and showed lower mean occupation ratio (0.3 ± 0.1 vs 0.6 ± 0.1) (all, p < .001). AUC for predicting insufficient repair was 0.945 for Goutallier grade, 0.961 for occupation ratio, 0.900 for muscle atrophy grade, 0.874 for mean elasticity, 0.971 for elasticity ratio, and 0.912 for gray-scale fatty infiltration grade. Elasticity ratio (cutoff ≥ 2.51) achieved sensitivity of 100.0% and specificity of 90.0% for insufficient repair. At multivariable analysis including tear size, the three MRI measures, elasticity ratio, and gray-scale fatty infiltration grade, the only independent predictors of insufficient repair were muscle atrophy grade of 2-3 (odds ratio [OR] = 9.3) and elasticity ratio (OR = 15.7). CONCLUSION. SWE-derived elasticity is higher in patients with insufficient rotator cuff repair; the elasticity ratio predicts insufficient repair independent of tear size and muscle characteristics. CLINICAL IMPACT. Preoperative SWE may serve as a prognostic marker in patients with rotator cuff tear.