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As one of the most prevalent chronic inflammatory skin diseases, atopic dermatitis (AD) increasingly affects the aging population. Amid the ongoing global aging trend, it's essential to recognize the intricate relationship between AD and aging. This paper reviews existing knowledge, summarizing clinical observations of associations between AD and aging-related diseases in various systems, including endocrine, cardiovascular, and neurological. Additionally, it discusses major theories explaining the correlation, encompassing skin-mucosal barriers, systemic inflammation and stress, genes, signal transduction, and environmental and behavioral factors. The association between AD and aging holds significant importance, both in population and basic perspectives. While further research is warranted, this paper aims to inspire deeper exploration of inflammation/allergy-aging dynamics and the timely management of elderly patients with AD. [ABSTRACT FROM AUTHOR]

Lactic acid (LA) is an essential glycolytic metabolite and energy source in the body, which is present in high levels in the synovial fluid of patients with rheumatoid arthritis (RA) and is a reliable indicator for identifying inflammatory arthritis. LA not only acts as an inflammatory amplifier in RA, recent studies have found that novel posttranslational modification (PTM) lactylation mediated by LA may also play a key role in RA. Single-cell sequencing showed that the RA lactylation score of patients with RA was significantly increased, and core lactylation-promoting genes, including NDUFB3, NGLY1, and other genes, were found to be potential biomarkers of RA. More studies have shown that lactylation can regulate genes in various cells, such as fibroblast-like synoviocytes (FLSs) and macrophages, thus playing a special role in the development and occurrence of autoimmune diseases, neurological diseases, and cancer diseases. In this paper, we review the research on lactylation in RA-related cells and mechanisms and bring new insights into the pathogenesis, diagnosis, and treatment of RA. [ABSTRACT FROM AUTHOR]

Globally, osteoarthritis is a common and highly disabling disease that places a heavy burden on society and medical systems. The role of biomechanical factors in the development of osteoarthritis has gradually received more attention. As a key biomechanical stimulus, fluid shear force is becoming the focus of research for its dual role in maintaining cartilage health and disease progression. This paper conducts an in-depth discussion on the mechanism of fluid shear force in osteoarthritis and its impact on the disease process, aiming to reveal how fluid shear stress affects the development of osteoarthritis by regulating the physiological function and signal transduction pathways of chondrocytes. [ABSTRACT FROM AUTHOR]

Heart failure (HF) represents a serious manifestation or advanced stage of various cardiac diseases. HF continues to impose a significant global disease burden, characterized by high rates of hospitalization and fatality. Furthermore, the pathogenesis and pathophysiological processes underlying HF remain incompletely understood, complicating its prevention and treatment strategies. One significant pathophysiological mechanism associated with HF is the systemic inflammatory response. PANoptosis, a novel mode of inflammatory cell death, has been extensively studied in the context of infectious diseases, neurodegenerative disorders, cancers, and other inflammatory conditions. Recent investigations have revealed that PANoptosis-related genes are markedly dysregulated in HF specimens. Consequently, the PANoptosis-mediated inflammatory response may represent a potential mechanism and therapeutic target for HF. This paper conducts a comprehensive analysis of the molecular pathways that drive PANoptosis. We discuss its role and potential therapeutic targets in HF, thereby providing valuable insights for clinical treatment and the development of novel therapies. [ABSTRACT FROM AUTHOR]

The gut microbiome (GM), often referred to as the second genome of the human body, plays a crucial role in various metabolic processes and mediates the development of numerous diseases. Intervertebral disc degeneration (IDD) is an age-related degenerative spinal disease characterized by the loss of disc height, hydration, and integrity, leading to pain and reduced mobility. Although the pathogenesis of IDD is not fully understood, recent studies suggest that dysbiosis of the gut microbiome may accelerate the progression of IDD through multiple mechanisms. This article begins by discussing the potential relationship between GM dysbiosis and human diseases, followed by a comprehensive review of the regulatory mechanisms of GM in skeletal diseases within the gut-disc axis framework. Furthermore, it explores three potential pathways through which GM dysbiosis may mediate the development of IDD: immunomodulation, bacterial translocation and colonization, and the decomposition and absorption of intestinal metabolites. These pathways can disrupt disc cell homeostasis and promote degenerative changes. Finally, this paper summarizes for the first time the potential therapeutic approaches for delaying IDD by targeting the gut-disc axis, providing new insights into the pathogenesis and regenerative repair strategies for IDD. [ABSTRACT FROM AUTHOR]

Lung diseases are associated with high morbidity and mortality rates, thereby jeopardizing human health and imposing a great burden on society. Currently, lung diseases are mainly treated with medications, oxygen therapy and mechanical ventilation, but these approaches are unable to effectively reduce the mortality rate. Therefore, lung transplantation remains the ultimate treatment for various chronic lung diseases, but this treatment is also hindered by the limited availability of lung sources, immature technology and a low survival rate after transplantation. With constant changes in the environment, pathogens, type and amount of harmful substances and the prevalence of respiratory diseases, there is an urgent need to identify alternative treatment methods. Research on stem cell therapy has been very successful in recent years, and mesenchymal stem cells (MSCs), together with their secretory bodies, play a significant therapeutic role. Extracellular vesicles of MSCs (MSC-EVs) are also major components of the paracrine secretion of MSCs, including exosomes, microvesicles, and apoptotic bodies, among which exosomes are the most typical. MSC-EVs are believed to be present in various tissues of the human body where they can carry proteins, DNA, RNA and biologically active factors, just to name a few. They can also transmit various biological signals to participate in different biological activities, including the maintenance of homeostasis within the tissue. Several studies have further demonstrated that MSCs and their generated extracellular vesicles play an important role in the treatment of diseases. In this paper, the origin, properties and roles of MSCs and MSC-EVs are reviewed, the mechanisms of different lung diseases, the limitations of current therapeutic options and the roles of MSC-EVs in Chronic Obstructive Pulmonary Disease, asthma, infectious lung disease, lung cancer, pulmonary fibrosis, pulmonary arterial hypertension, and acute lung injury/ acute respiratory distress syndrome are also discussed (Figure 1). In addition, the current limitations and possible future research directions are also discussed in view of providing new ideas for the role of MSC-EVs in the treatment of lung diseases. [ABSTRACT FROM AUTHOR]

The prevalence of urological malignancies continues to pose a significant global health challenge, particularly due to the poor prognosis associated with advanced stages of these diseases. Consequently, there is an urgent need to deepen our understanding of the molecular mechanisms governing the development of urological malignancies to facilitate breakthroughs in diagnosis and treatment. Pyroptosis, a novel and specific form of programmed cell death, plays a crucial role in regulating inflammatory responses, cell development, tissue homeostasis, and stress responses. Recent research has revealed a close association between pyroptosis and urological malignancies. In this paper, we review the pathogenesis and recent advancements in the understanding of pyroptosis in urological malignancies, elucidate the molecular mechanisms involved in its regulation, and aim to provide new directions for the clinical management of these diseases. [ABSTRACT FROM AUTHOR]

We believe there are serious problems with a recently published and highly publicized paper entitled "Serotonin reduction in post-acute sequelae of viral infection." The blood centrifugation procedure reportedly used by Wong et al would produce plasma that is substantially (over 95%) depleted of platelets. Given this, their published mean plasma serotonin values of 1.2 uM and 2.4 uM for the control/contrast groups appear to be at least 30 to 60 times too high and should be disregarded. The plasma serotonin values reported for the long COVID and viremia patients also should be disregarded, as should any comparisons to the control/contrast groups. We also note that the plasma serotonin means for the two control/contrast groups are not in good agreement. In the "Discussion" section, Wong et al state that their results tend to support the use of selective serotonin reuptake inhibitors (SSRIs) for the treatment of COVID-19, and they encourage further clinical trials of SSRIs. While they state that, "Our animal models demonstrate that serotonin levels can be restored and memory impairment reversed by precursor supplementation or SSRI treatment", it should be noted that no data are presented showing an increase or restoration in circulating serotonin with SSRI administration. In fact, one would expect a marked decline in platelet serotonin due to SSRIs' effective inhibition of the platelet serotonin transporter. Wong et al hypothesize that problems of long COVID arise from too little peripheral serotonin. However, given the frequent presence of a hyperaggregation state in long COVID, and the known augmenting effects of platelet serotonin on platelet aggregation, it is plausible to suggest that reductions in platelet serotonin might be associated with a lessening of the cardiovascular sequelae of COVID-19. [ABSTRACT FROM AUTHOR]

Long non-coding RNA (LncRNA), with transcripts over 200 nucleotides in length, play critical roles in numerous biological functions and have emerged as significant players in the pathogenesis of osteoarthritis (OA), an inflammatory condition traditionally viewed as a degenerative joint disease. This review comprehensively examines the influence of LncRNA on the inflammatory processes driving OA progression, focusing on their role in regulating gene expression, cellular activities, and inflammatory pathways. Notably, LncRNAs such as MALAT1, H19, and HOTAIR are upregulated in OA and exacerbate the inflammatory milieu by modulating key signaling pathways like NF-κB, TGF-β/SMAD, and Wnt/β-catenin. Conversely, LncRNA like MEG3 and GAS5, which are downregulated in OA, show potential in dampening inflammatory responses and protecting against cartilage degradation by influencing miRNA interactions and cytokine production. By enhancing our understanding of LncRNA' roles in OA inflammation, we can better leverage them as potential biomarkers for the disease and develop innovative therapeutic strategies for OA management. This paper aims to delineate the mechanisms by which LncRNA influence inflammatory responses in OA and propose them as novel targets for therapeutic intervention. [ABSTRACT FROM AUTHOR]

Atopic dermatitis (AD) is a chronic and inflammatory skin disease with intense itchiness that is highly prevalent worldwide.The pathogenesis of AD is complex and closely related to genetic factors, immunopathogenic factors, environmental factors, and skin infections. Mesenchymal stem cells (MSCs) are non-hematopoietic progenitor cells derived from the mesenchymal stroma. They have anti-inflammatory, anti-apoptotic, and regenerative properties. Numerous studies demonstrate that MSCs can play a therapeutic role in AD by regulating various immune cells, maintaining immune homeostasis, and promoting the repair of damaged tissues. The key mediators for their biological functions are extracellular vesicles (MSC-Evs) and soluble cytokines derived from MSCs. The safety and efficacy of MSCs have been demonstrated in clinical Phase I / IIa trials for AD. This paper provides a comprehensive review of the pathogenesis of AD and the currently published studies on the function of MSCs and MSC-Evs in AD, primarily including the pathogenesis and the immunomodulatory impacts of MSCs and MSC-Evs, along with advancements in clinical studies. It provides insights for comprehending AD pathogenesis and investigating treatments based on MSCs. [ABSTRACT FROM AUTHOR]

Sepsis is a severe systemic inflammatory response commonly occurring in infectious diseases, caused by infection with virulent pathogens. In the pathogenesis of sepsis, the cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) synthase-stimulator of interferon genes (cGAS-STING) signaling pathway serves a crucial role as a fundamental immunoregulatory mechanism. This signaling pathway activates STING upon recognizing intracellular DNA damage and pathogen-derived DNA, subsequently inducing the production of numerous inflammatory mediators, including interferon and inflammatory cytokines, which in turn trigger an inflammatory response. The aim of this paper is to explore the activation mechanism of the cGAS-STING signaling pathway in sepsis and its impact on inflammatory regulation. By delving into the mechanism of action of the cGAS-STING signaling pathway in sepsis, we aim to identify new therapeutic strategies for the treatment and prevention of sepsis. [ABSTRACT FROM AUTHOR]

During the past decade, mounting evidence has increasingly linked programmed cell death (PCD) to the progression and development of osteoarthritis (OA). There is a significant need for a thorough scientometric analysis that recapitulates the relationship between PCD and OA. This study aimed to collect articles and reviews focusing on PCD in OA, extracting data from January 1st, 2013, to October 31st, 2023, using the Web of Science. Various tools, including VOSviewer, CiteSpace, Pajek, Scimago Graphica, and the R package, were employed for scientometric and visualization analyses. Notably, China, the USA, and South Korea emerged as major contributors, collectively responsible for more than 85% of published papers and significantly influencing research in this field. Among different institutions, Shanghai Jiao Tong University, Xi'an Jiao Tong University, and Zhejiang University exhibited the highest productivity. Prolific authors included Wang Wei, Wang Jing, and Zhang Li. Osteoarthritis and Cartilage had the most publications in this area. Keywords related to PCD in OA prominently highlighted 'chondrocytes', 'inflammation', and 'oxidative stress', recognized as pivotal mechanisms contributing to PCD within OA. This study presents the first comprehensive scientometric analysis, offering a broad perspective on the knowledge framework and evolving patterns concerning PCD in relation to OA over the last decade. Such insights can aid researchers in comprehensively understanding this field and provide valuable directions for future explorations. [ABSTRACT FROM AUTHOR]

Rheumatic disease is a disease which is not yet fully clarified to etiology and also involved in a local pathological injury or systemic disease. With the continuous improvement of clinical medical research in recent years, the development process of rheumatic diseases has been gradually elucidated; with the intensely study of epigenetics, it is realized that environmental changes can affect genetics, among which histone acetylation is one of the essential mechanisms in epigenetics. Histone deacetylases (HDACs) play an important role in regulating gene expression in various biological processes, including differentiation, development, stress response, and injury. HDACs are involved in a variety of physiological processes and are promising drug targets in various pathological conditions, such as cancer, cardiac and neurodegenerative diseases, inflammation, metabolic and immune disorders, and viral and parasitic infections. In this paper, we reviewed the roles of HDACs in rheumatic diseases in terms of their classification and function. [ABSTRACT FROM AUTHOR]

Introduction: This paper focuses on the expression and role of FcγRIIb in neuroinflammation, exploring the molecular mechanisms by which FcγRIIb interacts with the bridging protein DAP12 to regulate the PI3K-AKT signaling pathway that promote neuroinflammation and aggravate neuronal injury.Methods: LPS-induced neuroinflammation models in vivo and in vitro were constructed to explore the role and mechanism of FcγRIIb in CNS inflammation. Subsequently, FcγRIIb was knocked down or overexpressed to observe the activation of BV2 cell and the effect on PI3K-AKT pathway. Then the PI3K-AKT pathway was blocked to observe its effect on cell activation and FcγRIIb expression. We analyzed the interaction between FcγRIIb and DAP12 by Immunoprecipitation technique. Then FcγRIIb was overexpressed while knocking down DAP12 to observe its effect on PI3K-AKT pathway. Finally, BV2 cell culture supernatant was co-cultured with neuronal cell HT22 to observe its effect on neuronal apoptosis and cell activity.Results: In vivo and in vitro, we found that FcγRIIb expression was significantly increased and activated the PI3K-AKT pathway. Contrary to the results of overexpression of FcγRIIb, knockdown of FcγRIIb resulted in a significant low level of relevant inflammatory factors and suppressed the PI3K-AKT pathway. Furthermore, LPS stimulation induced an interaction between FcγRIIb and DAP12. Knockdown of DAP12 suppressed inflammation and activation of the PI3K-AKT pathway in BV2 cells, and meantime overexpression of FcγRIIb suppressed the level of FcγRIIb-induced AKT phosphorylation. Additionally, knockdown of FcγRIIb inhibited microglia activation, which induced neuronal apoptosis.Discussion: Altogether, our experiments indicate that FcγRIIb interacts with DAP12 to promote microglia activation by activating the PI3K-AKT pathway while leading to neuronal apoptosis and exacerbating brain tissue injury, which may provide a new target for the treatment of inflammatory diseases in the central nervous system. [ABSTRACT FROM AUTHOR]

Purpose: Intervertebral disc degeneration (IDD) is considered the predominant cause of low back pain (LBP) and accounts for global disability and a substantial socioeconomic burden. Given the unsatisfactory outcomes of current treatment strategies, cartilage endplate-derived stem cells (CESCs) are increasingly used in intervertebral disc regeneration. However, comprehensive analyses on CESCs remain rare. Herein, we examined the biological functions and applications of CESCs in IDD.Methods: PubMed, Embase, and Cochrane Library databases were searched to identify studies focused on CESCs. Relevant information from included studies was extracted. Descriptive statistics were performed. Correlation analysis was conducted to determine the relationship among Web of Science (WoS) citations, Dimensions, and Altmetric Attention Score (AAS).Results: Twenty-six studies were included in this study. Most studies (n=20) isolated CESCs from humans, followed by rats (n=5) and rabbits (n=1). Twenty studies were performed in vitro, and the remaining six were implemented both in vivo and in vitro. The findings of this study provide insight into the biological properties of CESCs and clarify their potential application for intervertebral disc regeneration. There was a very high correlation between WoS and Dimensions citation count (p< 0.001, r=0.988).Conclusion: This study, for the first time, elaborates biological features of CESCs and analyzes their potential applications in regenerating intervertebral discs. CESCs may be promising candidates for protecting the intervertebral disc from degeneration and contributing to intervertebral disc regeneration. [ABSTRACT FROM AUTHOR]

Diabetic kidney disease (DKD) is one of the prime causes of end-stage renal disease. At present, the treatment of DKD is mainly confined to inhibiting the renin-angiotensin-aldosterone system, but the therapeutic effects is not satisfactory. As a kind of very rare and precious medicinal fungi, Inonotus obliquus has a very high medicinal value. Due to its special hypoglycemic and pharmacological effect, researchers currently have attached great importance to it. In this paper, the biological activities, pharmacological effects and application status in the treatment of DKD-related diseases of Inonotus obliquus and the latest progress of metabolites isolated from it in DKD were summarized, thus providing detailed insights and basic understanding of the potential application prospects in DKD. [ABSTRACT FROM AUTHOR]

Ferroptosis is a novel way of regulating cell death, which occurs in a process that is closely linked to intracellular iron metabolism, lipid metabolism, amino acid metabolism, and multiple signaling pathways. The latest research shows that ferroptosis plays a key role in the pathogenesis of acute kidney injury (AKI). Ferroptosis may be an important target for treating AKI caused by various reasons, such as ischemia-reperfusion injury, rhabdomyolysis syndrome, sepsis, and nephrotoxic drugs. This paper provides a review on the regulatory mechanisms of ferroptosis and its role in AKI, which may help to provide new research ideas for the treatment of AKI and future research. [ABSTRACT FROM AUTHOR]

This document is a corrigendum for an article titled "S100A9 as a Key Myocardial Injury Factor Interacting with ATP5 Exacerbates Mitochondrial Dysfunction and Oxidative Stress in Sepsis-Induced Cardiomyopathy." The authors acknowledge an error in Figure 8A of the original article, specifically in the merge image of the S100A9KD-lps group. The correct Figure 8 is provided in the corrigendum. The authors apologize for the error and state that it does not affect the results and conclusions of the paper. [Extracted from the article]

The interrelations and sequencing of interleukins are complex (inter)actions where each interleukin can stimulate the secretion of its preceding interleukin. In this paper, we attempt to summarize the currently known roles of IL-4, IL-13, IL-31, and IL-33 from a multi-disciplinary perspective. In order to conduct a comprehensive review of the current literature, a search was conducted using PubMed, Google Scholar, Medscape, UpToDate, and Key Elsevier for keywords. The results were compiled from case reports, case series, letters, and literature review papers, and analyzed by a panel of multi-disciplinary specialist physicians for relevance. Based on 173 results, we compiled the following review of interleukin signaling and its clinical significance across a multitude of medical specialties. Interleukins are at the bed rock of a multitude of pathologies across different organ systems and understanding their role will likely lead to novel treatments and better outcomes for our patients. New interleukins are being described, and the role of this inflammatory cascade is still coming to light. We hope this multi-discipline review on the role interleukins play in current pathology assists in this scope. [ABSTRACT FROM AUTHOR]

Spinal Cord Injury (SCI), with its morbidity characteristics of high disability rate and high mortality rate, is a disease that is highly destructive to both the physiology and psychology of the patient, and for which there is still a lack of effective treatment. Following spinal cord injury, a cascade of secondary injury reactions known as ischemia, peripheral inflammatory cell infiltration, oxidative stress, etc. create a microenvironment that is unfavorable to neural recovery and ultimately results in apoptosis and necrosis of neurons and glial cells. Mesenchymal stem cell (MSC) transplantation has emerged as a more promising therapeutic options in recent years. MSC can promote spinal cord injury repair through a variety of mechanisms, including immunomodulation, neuroprotection, and nerve regeneration, giving patients with spinal cord injury hope. In this paper, it is discussed the neuroprotection and nerve regeneration components of MSCs' therapeutic method for treating spinal cord injuries. [ABSTRACT FROM AUTHOR]

Cholestasis is a common clinical event in which bile formation and excretion are blocked, leading to retention of bile acids or bile salts; whether it occurs intra- or extrahepatically, primary or secondary, its pathogenesis is still unclear and is influenced by a combination of factors. In a variety of inflammatory and immune cells such as neutrophils, macrophages (intrahepatic macrophages are also known as Kupffer cells), mast cells, NK cells, and even T cells in humoral immunity and B cells in cellular immunity, inflammation can be a "second strike" against cholestatic liver injury. These cells, stimulated by a variety of factors such as bile acids, inflammatory chemokines, and complement, can be activated and accumulate in the cholestatic liver, and with the involvement of inflammatory mediators and modulation by cytokines, can lead to destruction of hepatocytes and bile duct epithelial cells and exacerbate (and occasionally retard) the progression of cholestatic liver disease. In this paper, we summarized the new research advances proposed so far regarding the relationship between inflammation and cholestasis, aiming to provide reference for researchers and clinicians in the field of cholestatic liver injury research. [ABSTRACT FROM AUTHOR]

Peri-implantitis is an important cause of oral implant failure. In the past, TLR4 and TLR2 in the Toll-like family were generally considered as the key immune recognition receptors regulating peri-implantitis. However, under the guidance of this theory, there are still some unexplainable peri-implantitis symptoms. With the discovery of novel intracellular LPS receptor Caspase-11, a new understanding of inflammatory signaling and immune regulation in the development of peri-implantitis has been gained. However, the regulatory role of Caspase-11 in peri-implantitis and its crosstalk with the TLR4 pathway remain unclear. The therapeutic effect of drugs targeting Caspase-11 on peri-implantitis is still in its early stages. In view of this situation, this paper reviews the possible role of Caspase-11 in peri-implant inflammation, elaborated the entry process of LPS and the activation mechanism of Caspase-11, and analyzes the differences in Caspase-11 between commonly studied animals, mice and humans. The current research hotspots and challenges are also analyzed to provide new insights and ideas for researchers. [ABSTRACT FROM AUTHOR]

Since the incidence of gouty arthritis (GA) exhibits yearly increases, accurate assessment and early treatment have significant values for improving disease conditions and monitoring prognosis. Neutrophil to lymphocyte ratio (NLR) is a common indicator in blood routine, which has the characteristics of easy access and low cost. In recent years, NLR has been proven to be an effective indicator for guiding the diagnosis, treatment, and prognosis of various diseases. Moreover, NLR has varying degrees of relationship with various inflammatory biomarkers, which can affect and reflect the inflammatory response in the body. This paper reviews the independent value of NLR for GA and its underlying molecular pathological mechanisms, intending to contribute to the further application of NLR. [ABSTRACT FROM AUTHOR]

Ferroptosis, a programmed cell death discovered in recent years, is an iron-dependent lipid peroxidation accumulation. Unlike other modes of cell death (autophagy, necroptosis, pyroptosis, cuproptosis, etc.), ferroptosis has unique morphological characteristics and plays an important role in a variety of diseases. In recent years, there has been great progress in the study of ferroptosis. Studies have found that ferroptosis is associated with acute lung injury (ALI), a condition with a high mortality rate and limited treatment options. This paper summarizes the mechanism of ferroptosis from the perspectives of iron metabolism, lipid metabolism, amino acid metabolism, and glutathione metabolism. It also discusses the research progress of ferroptosis in ALI in order to find new directions for the prevention and treatment of this condition. [ABSTRACT FROM AUTHOR]

All humans are universally affected by inflammatory diseases, and there is an urgent need to identify new anti-inflammatory drugs with good therapeutic benefits and minimal side effects to the organism. Recently, it has been found that plant-derived vesicle-like nanoparticles (PDVLNs) have good biocompatibility, with their active ingredients exhibiting good therapeutic effects on inflammation. They can also be used as drug carriers for targeted delivery of anti-inflammatory drugs. Therefore, PDVLNs represent a popular research area for novel anti-inflammatory drugs. This paper details the origin, biological functions, isolation and purification, and identification of PDVLNs, as well as the therapeutic effects of their intrinsic bioactive components on inflammatory diseases. It also introduces their targets as drug carriers to facilitate the development and application of PDVLNs anti-inflammatory drugs. [ABSTRACT FROM AUTHOR]

Toll-like receptor 5 (TLR5) is a pattern recognition receptor that specifically recognizes flagellin and consequently plays a crucial role in the control of intestinal homeostasis by activating innate and adaptive immune responses. TLR5 overexpression, on the other hand, might disrupt the intestinal mucosal barrier, which serves as the first line of defense against harmful microbes. The intestine symbiotic bacteria, mucous layer, intestinal epithelial cells (IECs), adherens junctions (such as tight junctions and peripheral membrane proteins), the intestinal mucosal immune system, and cytokines make up the intestinal mucosal barrier. Impaired barrier function has been linked to intestinal illnesses such as inflammatory bowel disease (IBD). IBD is a persistent non-specific inflammatory illness of the digestive system with an unknown cause. It is now thought to be linked to infection, environment, genes, immune system, and the gut microbiota. The significance of immunological dysfunction in IBD has received more attention in recent years. The purpose of this paper is to explore TLR5's position in the intestinal mucosal barrier and its relevance to IBD. [ABSTRACT FROM AUTHOR]

Autophagy is a highly conserved process that maintains cell stability in eukaryotes, participates in the turnover of intracellular substances to maintain cell function, helps to resist pathogen invasion, and improves cell tolerance to environmental changes. Autophagy has been observed in many diseases, and the symptoms of these diseases are significantly improved by regulating autophagy. Autophagy is also involved in the development of lung diseases. Studies have shown that autophagy may play a beneficial or harmful role in acute lung injury (ALI), and ALI has been treated with traditional Chinese medicine designed to promote or inhibit autophagy. In this paper, the molecular mechanism and common pathways regulating autophagy and the relationship between autophagy and ALI are introduced, and the active ingredients of traditional Chinese medicine that improve ALI symptoms by regulating autophagy are summarized. [ABSTRACT FROM AUTHOR]

Purpose: The objective of this paper is to explore the role of circHECTD1 in vascular smooth muscle cells (VSMCs) and atherosclerosis (AS). Methods: VSMCs were treated with platelet-derived growth factor-BB (PDGF-BB) in vitro, and the level of circHECTD1 was determined using qRT-PCR. Cell proliferation, migration, and invasion were analyzed using CCK8 and transwell assays. Cell apoptosis and cell cycle were analyzed using flow cytometry. The binding interaction between circHECTD1 and KHDRBS3 or EZH2 was investigated using the RIP, RNA pull-down. Results: CircHECTD1 was upregulated in PDGF-BB-induced VSMCs with a dose-dependent and time-dependent manner. Knockdown of circHECTD1 suppressed VSMCsproliferation and migration and enhanced cell apoptosis in VSMCs, while circHECTD1 overexpression yielded opposite effects. Mechanistically, circHECTD1 could interact with KHDRBS3, thus enhanced the stability of EZH2 mRNA and increased EZH2 protein level. In addition, silencing EZH2 in VSMCs reversed the proliferation-enhancing effect of circHECTD1 overexpression. Conclusion: Our findings provided providing a potential prognostic and therapy biomarker for AS. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by polyarticular, symmetric, and aggressive inflammation of the small joints in the hands and feet, resulting in dysfunction. With progress and development in medicine, treatment of RA is constantly evolving, making several drugs available for the treatment of RA. From the nonsteroidal anti-inflammatory drugs (NSAIDs) at the start of illness to glucocorticoids and then to conventional synthetic DMARDs (csDMARDs), biologic DMARDs (bDMARDs), and targeted synthetic DMARDs (tsDMARDs), therapeutic-use drugs for RA have been keeping pace with scientific research. However, various types of drugs have additional side effects when used over the long-term. New and emerging biological and targeted agents have been widely applied in recent years; however, the side effects have not been thoroughly investigated. In this paper, we review the research progress on liver damage caused by novel biological and targeted agents available for RA treatment. The aim is to provide a reference for rational clinical administration of such drugs. [ABSTRACT FROM AUTHOR]

Read the original articleXie NQ, Zhang YL, Zheng ZL, Zheng QL, Chen RJ. J Inflamm Res. 2023;16:6319–6328.The authors have advised that they neglected to include a funding statement on page 6327 of the published paper. The funding statement should read as follows.FundingThis work was supported by Quanzhou Medical College research project (XYL2305).The authors apologize for this error.By Ning-Qiu Xie; Yu-Lin Zhang; Zi-Li Zheng; Quan-Lin Zheng and Ruo-Ji ChenReported by Author; Author; Author; Author; Author [Extracted from the article]

WKYMVm (Trp-Lys-Tyr-Met-Val-D-Met) is a synthetic hexapeptide identified as a potent agonist of FPRs. FPRs are widely expressed on the cell membrane of immune cells. Therefore, WKYMVm participates in the regulation of immune cells by activating FPRs, and plays a therapeutic role in infections, tumors, autoimmune diseases and so on. WKYMVm can promote the chemotactic migration, increase the bactericidal activity of neutrophils and monocytes. WKYMVm also regulates the number and polarization of macrophages, affects the maturation of DCs and the differentiation of T cells, and promotes the activation and chemotaxis of NK cells. These functions make WKYMVm a candidate drug for immunotherapy. In this paper, we summarize the regulatory effects and underlying mechanisms of WKYMVm on six immune cells (neutrophils, monocytes, macrophages, DCs, T cells and NK cells) to increase comprehensive understanding and promote further research on WKYMVm. [ABSTRACT FROM AUTHOR]

The link between inflammation and cancer is still an attractive subject of many studies because systemic inflammatory response has been proven to play a pivotal role in cancer progression and metastasis. The strongest relationship between chronic inflammation and cancer development is observed in colorectal cancer (CRC). The evaluation of ratios derived from the routinely performed inflammatory biomarkers shows limited performances and limited clinical utility when individually used as prognostic factors for patients with CRC. In this review, we would like to summarize the latest knowledge about the diagnostic utility of systemic inflammatory ratios: neutrophil/lymphocyte (NLR), lymphocyte/monocyte (LMR), and platelet/lymphocyte (PLR) in CRC. We focused on the papers that assessed the diagnostic utility of blood cell parameters on the basis of the area under the ROC curve published in the recent 6 years. Identification of biomarkers that are significantly associated with prognostic in cancer would help the selection of patients with a high risk of poor outcomes. [ABSTRACT FROM AUTHOR]

Sepsis is a common and fatal disease, especially in critically ill patients. Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction with acute altered consciousness, permanent cognitive impairment, and even coma, accompanied by sepsis, without direct central nervous system infection. When managing SAE, early identification and quantification of axonal damage facilitate faster and more accurate diagnosis and prognosis. Although no specific markers for SAE have been identified, several biomarkers have been proposed. Neurofilament light chain (NFL) is a highly expressed cytoskeletal component of neurofilament (NF) proteins that can be found in blood and cerebrospinal fluid (CSF) after exposure to axonal injury. NFs can be used as diagnostic and prognostic biomarkers for sepsis-related brain injury. Phosphorylation of NFs contributes to the maturation and stabilization of cytoskeletal structures, especially axons, and facilitates axonal transport, including mitochondrial transport and energy transport. The stability of NF proteins can be assessed by monitoring the expression of NF genes. Furthermore, phosphorylation levels of NFs can be monitored to determine mitochondrial axonal transport associated with cellular energy metabolism at distal axons to assess progression during SAE treatment. This paper provides new insights into the biological characteristics, detection techniques, and scientific achievements of NFs, and discusses the underlying mechanisms and future research directions of NFs in SAE. Graphical [ABSTRACT FROM AUTHOR]

Trillions of microorganisms exist in the human intestine as commensals and contribute to homeostasis through their interactions with the immune system. In this review, we use previous evidence from published papers to elucidate the involvement of commensal-specific T cells (CSTCs) in regulating intestinal inflammatory responses. CSTCs are generated centrally in the thymus or peripherally at mucosal interfaces and present as CD4+ or CD8+ T cells. Bacteria, fungi, and even viruses act commensally with humans, warranting consideration of CSTCs in this critical relationship. Dysregulation of this immunological balance can result in both intestinal inflammation or damaging autoimmune responses elsewhere in the body. Given the relative novelty of CSTCs in the literature, we aim to introduce the importance of their role in maintaining immune homeostasis at barrier sites such as the intestine. [ABSTRACT FROM AUTHOR]

Purpose: As an inflammatory form of programmed cell death, pyroptosis has been well established to be associated with tumorigenesis and tumor immune microenvironment. In this paper, we aimed at the construction of a pyroptosis-related gene prognostic index (PRGPI) for predicting prognosis and guiding individualized immunotherapy in glioma patients. Patients and Methods: Pyroptosis-related genes (PRGs) were identified based on a detailed review of published literatures. The transcriptome data and clinical information of glioma patients were obtained from CGGA and TCGA databases. PRGPI was constructed by using the multivariate Cox regression method. The immune cell infiltration level was analyzed via CIBERSORT algorithm. The tumor immune dysfunction and exclusion (TIDE) algorithm was applied to evaluate the potential response to immune checkpoint inhibitor (ICI) therapy. The expression patterns of PRGs in PRGPI were validated in cell lines and pathological specimens. Results: We identified a total of 31 PRGs. Among them, PRGs (CASP3, DPP9, MAPK8, PELP1 and TOMM20) were selected for the construction of PRGPI. In both training (CGGA693) and validation (CGGA325 and TCGA) cohorts, PRGPI-high patients showed an inferior survival outcome compared with PRGPI-low patients. ROC curves illustrated that the prognostic prediction power of PRGPI was robust. A nomogram was developed based on independent prognostic indicators (PRGPI, age and WHO grade), and also exhibited a strong forecasting ability for overall survival (OS). Additionally, PRGPI-high patients exhibited higher immune, stroma and ESTIMATE scores, lower tumor purity, higher infiltration of M2-type macrophages, lower infiltration of CD8+ T cells and activated NK cells, higher tumor mutation burden (TMB), and higher expression of immune checkpoints. TIDE showed that PRGPI-high group had more responders of ICI therapy than PRGPI-low group. Finally, the expression patterns of five selected PRGs in PRGPI were significantly different between normal and glioma. Conclusion: The constructed PRGPI can be used for predicting prognosis and guiding individualized immunotherapy in glioma patients. [ABSTRACT FROM AUTHOR]

Sepsis is a major immune response disorder caused by infection, with very high incidence and mortality rates. In the clinic, sepsis and its complications are mainly controlled and treated with antibiotics, anti-inflammatory, and antioxidant drugs. However, these treatments have some shortcomings, such as rapid metabolism and severe side effects. The emergence of drug delivery nanosystems can significantly improve tissue permeability, prolong drugs' circulation time, and reduce side effects. In this paper, we reviewed recent drug delivery nanosystems designed for sepsis treatment based on their mechanisms (anti-bacterial, anti-inflammatory, and antioxidant). Although great progress has been made recently, clinical practice transformation is still very difficult. Therefore, we also discussed key obstacles, including tissue distribution, overcoming bacterial resistance, and single treatment modes. Finally, a rigorous optimization of drug delivery nanosystems is expected to present great potential for sepsis therapy. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is common in immune-mediated inflammatory diseases (IMIDs) and it is predominately attributed to the interplay between chronic inflammation and traditional CVD risk factors. CVD has significant impact on the survival of patients with IMIDs as it is associated with increased morbidity and mortality. Despite recommendations for monitoring and managing CVD in patients with IMIDs, the individual CVD risk assessment remains problematic as CVD risk calculators for the general population consistently underestimate the risk in patients with IMIDs. Application of new technologies utilizing artificial intelligence techniques have shown promising potential for tailoring predictive medicine to the individual patient, but further validation of their role in clinical decision-making is warranted. In the meantime, individuals with IMIDs should be encouraged to adopt behavioral interventions targeting at modifiable lifestyle CVD risk factors, whereas rheumatologists need to be well aware of the unfavorable effects of antirheumatic medication on various CVD risk factors and outcomes. In the current paper, we aim to provide an overview of current and emerging strategies for mitigating CVD risk in patients with IMIDs, based on a practical approach. [ABSTRACT FROM AUTHOR]

The article "Interplay of TLR4 and SARS-CoV-2: Possible Involvement of microRNAs" discusses the potential role of microRNAs in regulating Toll-like Receptor 4 (TLR4) gene expression and its impact on the severity of COVID-19 infections. The authors suggest that targeting TLR4 with microRNA molecules could inhibit its activity, reducing the upregulation of pro-inflammatory genes and improving patient outcomes. Further research is needed to explore the therapeutic potential of "microRNA therapeutics" in the context of SARS-CoV-2 infection. [Extracted from the article]

The article discusses the association between Stress Hyperglycemia Ratio (SHR) and in-hospital mortality in patients with sepsis, highlighting the importance of timely identification of high-risk patients. The study utilized various analytical methods to establish a relationship between SHR and mortality, providing valuable insights for clinical decision-making. While the study design and methodology were sound, suggestions for improvement include considering competing risk models, expanding covariates to include factors like alcohol consumption, and providing rationale for subgroup analyses. The article emphasizes the need for healthcare professionals to enhance the management of septic patients to reduce the burden on global health systems. [Extracted from the article]

Various nonsteroidal anti-inflammatory drugs have been shown to reduce pain and inflammation by blocking the metabolism of arachidonic acid by isoform of cyclooxygenase enzyme, thereby reducing the production of prostaglandin. Sadly, there are many side effects associated with the administration of nonsteroidal anti-inflammatory drugs. However, there are medicinal plants with anti-inflammatory therapeutic effects with low or no side effects. The African continent is richly endowed with diverse medicinal plants with anti-inflammatory activities that have been shown to be effective in the treatment of inflammatory conditions in traditional medicine. Interestingly, scientists have examined some of these African medicinal plants and documented their biological and therapeutic activities. Unfortunately, medicinal plants from different countries in Africa with anti-inflammatory properties have not been documented in a single review paper. It is important to document the ethnobotanical knowledge and applications of anti-inflammatory medicinal plants from selected countries representing different regions of the African continent. This paper therefore documents anti-inflammatory activities of various medicinal plants from different geographical regions of Africa with the aim of presenting the diversity of medicinal plants that are of traditional or therapeutic use in Africa. [ABSTRACT FROM AUTHOR]

Introduction: COVID-19 poses a chronic threat to inflammatory systems, reinforcing the need for efficient anti-inflammatory strategies. The purpose of this review and analysis was to determine the efficacy of various interventions upon the inflammatory markers most affected by COVID-19. The focus was on the markers associated with COVID-19, not the etiology of the virus itself. Methods: Based on 27 reviewed papers, information was extracted on the effects of COVID-19 upon inflammatory markers, then the effects of standard treatments (Remdesivir, Tocilizumab) and adjunctive interventions (vitamin D3, melatonin, and meditation) were extracted for those markers. These data were used to approximate effect sizes for the disease or interventions via standardized mean differences (SMD). Results: The data that were available indicated that adjunctive interventions affected 68.4% of the inflammatory markers impacted by COVID-19, while standard pharmaceutical medication affected 26.3%. Discussion: Nonstandard adjunctive care appeared to have comparable or superior effects in comparison to Remdesivir and Tocilizumab on the inflammatory markers most impacted by COVID-19. Alongside standards of care, melatonin, vitamin D3, and meditation should be considered for treatment of SARS-COV-2 infection and COVID-19 disease. [ABSTRACT FROM AUTHOR]

Background: Interleukin-33 (IL-33) is an alarmin that is released following cellular damage, mechanical injury, or necrosis. It is a member of the IL-1 family and binds to a heterodimer receptor consisting of ST2 and IL-1RAP to induce the production of a wide range of cellular mediators, including the type 2 cytokines IL-4, IL-5 and IL-13. This relationship has led to the hypothesis that the IL-33/ST2 pathway is a driver of allergic disease and inhibition of the IL-33 and ST2 association could have therapeutic benefit. Methods: In this paper, we describe the selection of a phage antibody through the ability to bind human IL-33 and block IL-33/ST2 interaction. This hit antibody was then affinity matured by site-directed mutagenesis of the antibody complementarity-determining regions (CDRs). Further characterization of a fully human monoclonal antibody (mAb), torudokimab (LY3375880) included demonstration of human IL-33 neutralization activity in vitro with an NFκB reporter assay and IL-33 induced mast cell cytokine secretion assay, followed by an in vivo IL-33-induced pharmacodynamic inhibition assay in mice that used IL-5 production as the endpoint. Results: Torudokimab is highly specific to IL-33 and does not bind any of the other IL-1 family members. Furthermore, torudokimab binds human and cynomolgus monkey IL-33 with higher affinity than the binding affinity of IL-33 to ST2, but does not bind mouse, rat, or rabbit IL-33. Torudokimab's half-life in cynomolgous monkey projects monthly dosing in the clinic. Conclusion: Due to torudokimab's high affinity, its ability to completely neutralize IL-33 activity in vitro and in vivo, and the observed cynomolgus monkey pharmacokinetic properties, this molecule was selected for clinical development. [ABSTRACT FROM AUTHOR]

Figure 6C, p-NF- B, Hippocampus, P8, appears to have been duplicated with the same image from Figure 10F, COX-2, Hippocampus, Ethanol + DNP from Ullah et al, 2022 (https://doi.org/10.2147/JIR.S351913). Specifically, Figure 4E, Hippocampus, P9, appears to have been duplicated with the same image from Figure 8E, Hippocampus, Ethanol + DNP from Ullah et al, 2022 (https://doi.org/10.2147/JIR.S351913). This retraction relates to this paper Naz S, Al Kury LT, Nadeem H, et al. I J Inflamm Res i . 2022;15:3643-3660. [Extracted from the article]

This retraction relates to this paper Ullah A, Al Kury LT, Althobaiti YS, Ali T, Shah FA. Figure 10D, TNF- , Hippocampus, Ethanol, appears to have been duplicated with the same image from Figure 10F, COX-2, Hippocampus, Ethanol. [Extracted from the article]

Methylation, first proposed in DNAs, but later found in RNAs, serves as one of the most widespread epigenetic modifications in eukaryotes, where N6-methyladenosine (m6A) modification has been found to play an important role in a variety of cancers including colorectal cancer (CRC). Under the action of various enzymes and proteins, the regulatory role of m6A in RNAs and immune cells has also been gradually realized. This paper reviews the general biogenesis and effects of m6A, and its emerging crucial role in intestinal mucosal immunity via the regulation of RNAs and immune cells, and thus closely related to the occurrence and development of inflammatory bowel disease (IBD) and CRC. m6A-related genes and regulatory factors are expected to be potential predictive markers and therapeutic targets. [ABSTRACT FROM AUTHOR]

Pyroptosis is a kind of pro-inflammatory cell death. Compared with autophagy and apoptosis, pyroptosis has unique characteristics in morphology and mechanism. Specifically, pyroptosis is a kind of cell lysis mediated by the Gasdermin family, releases inflammatory cytokines IL-1β and IL-18. There are three different forms of mechanism, which are caspase-1-mediated, caspase-4/5/11-mediated and caspase-3-mediated. A large number of studies have proved that pyroptosis is closely related to cardiovascular disease. This paper reviewed the recent progress in the related research on pyroptosis and myocardial infarction, ischemia-reperfusion, atherosclerosis, diabetic cardiomyopathy, arrhythmia, heart failure hypertension and Kawasaki disease. Therefore, we believe that pyroptosis may be a new therapeutic target in the cardiovascular field. [ABSTRACT FROM AUTHOR]

In an earlier publication a binary model for chronic diseases classification has been proposed. According to the model, chronic diseases were classified as "high Treg" or "low Treg" diseases, depending on whether the immune response is anti- or pro-inflammatory and assuming that regulatory T cells are major determinants of the response. It turned out that most cancers are "high Treg" diseases, while autoimmune diseases are "low Treg". This paper proposes a molecular cause for this binary response. The mechanism proposed depends on the effect of protein kinases on the immune system. Thus, protein kinases are classified as anti- or pro-inflammatory kinases depending on whether they drive "high Treg" or "low Treg" diseases. Observations reported in the earlier publication can be described in terms of anti-inflammatory kinase (AIK) or pro-inflammatory kinase (PIK) activity. Analysis of literature data reveals that the two classes of kinases display distinctive properties relating to their interactions with pathogens and environmental factors. Pathogens that promote Treg activity ("high Treg" pathogens) activate AIKs, while pathogens that suppress Treg activity ("low Treg" pathogens) activate PIKs. Diseases driven by AIKs are associated with "high Treg" pathogens while those diseases driven by PIKs are associated with "low Treg" pathogens. By promoting the activity of AIKs, alcohol consumption increases the risk of "high Treg" cancers but decreases the risk of some "low Treg" autoimmune diseases. JAK1 gain-of-function mutations are observed at high frequencies in autoimmune diseases while JAK1 loss-of-function mutations are observed at high frequencies in cancers with high tumor-infiltrating Tregs. It should also be noted that the corresponding two classes of protein kinase inhibitors are mutually exclusive in terms of their approved therapeutic indications. There is no protein kinase inhibitor that is approved for the treatment of both autoimmune diseases and "high Treg" cancers. Although there are exceptions to the conclusions presented above, these conclusions are supported by the great bulk of published data. It therefore seems that the binary division of protein kinases is a useful tool for elucidating (at the molecular level) many distinctive properties of cancers and autoimmune diseases. [ABSTRACT FROM AUTHOR]

Initially, the SARS-CoV-2 virus was considered as a pneumonia virus; however, a series of peer reviewed medical papers published in the last eight months suggest that this virus attacks the brain, heart, intestine, nervous and vascular systems, as well the blood stream. Although many facts remain unknown, an objective appraisal of the current scientific literature addressing the latest progress on COVID-19 is required. The aim of the present study was to conduct a critical review of the literature, focusing on the current molecular structure of SARS-CoV-2 and prospective treatment modalities of COVID-19. The main objectives were to collect, scrutinize and objectively evaluate the current scientific evidence-based information, as well to provide an updated overview of the topic that is ongoing. The authors underlined potential prospective therapies, including vaccine and phototherapy, as a monotherapy or combined with current treatment modalities. The authors concluded that this review has produced high quality evidence, which can be utilized by the clinical scientific community for future reference, as the knowledge and understanding of the SARS-CoV-2 virus are evolving, in terms of its epidemiological, pathogenicity, and clinical manifestations, which ultimately map the strategic path, towards an effective and safe treatment and production of a reliable and potent vaccine. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the association between vitamin D and molecules related to vitamin D metabolism in children with sepsis. Methods: A total of 98 hospitalized children with sepsis were included in this study. Blood samples were collected within the first 4 h of admission. Blood vitamin D; molecules related to vitamin D metabolism including vitamin-D-binding protein (VDBP), 7-dehydrocholesterol reductase (DHCR7), 25-hydroxylase (CYP2R1), 24-hydroxylase (CYP24A1), and cathelicidin (CATH); and other inflammatory markers including interleukin-6 (IL-6), procalcitonin (PCT), C-reactive protein (CRP), and white blood cell count (WBC) were measured. Results: Of the enrolled children, 23.47% (23/98) were confirmed to have severe sepsis, and 10.20% (10/98) died. The prevalence of hypovitaminosis D was 46.94% (46/98) in the children with sepsis. Children with hypovitaminosis D had lower levels of CYP2R1 and CATH and higher levels of CYP24A1, PCT, and IL-6 compared to children with vitamin D sufficiency. Blood vitamin D level was positively correlated with blood VDBP, CYP2R1, and CATH and negatively correlated with CYP24A1, PCT, and IL-6. Blood vitamin D was not independently associated with severe sepsis and mortality, but it was independently associated with the requirement of intensive care unit (ICU) stay. Conclusion: Molecules related to vitamin D metabolism such as VDBP, CYP2R1, and CYP24A1 are involved in regulating the levels of circulating vitamin D. Children with sepsis had a high prevalence of hypovitaminosis D. Hypovitaminosis D was independently associated with the requirement of ICU stay in children with sepsis. [ABSTRACT FROM AUTHOR]