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Fibroblasts, the principal cellular mediators of connective tissue remodeling, play a crucial role in the formation of physiological and pathological scars. Understanding the intricate interplay between fibroblasts and other cellular and molecular components is essential for elucidating the underlying mechanisms driving scar formation. Hypertrophic scars, keloids and atrophic scars arise from dysregulated wound healing processes characterized by persistent inflammation, aberrant collagen deposition, and impaired extracellular matrix remodeling. Fibroblasts play a central role in the pathogenesis of such pathological scars, driving aberrant extracellular matrix remodeling, subsequently contributing to the formation of raised or depressed fibrotic lesions. The investigation of complex interactions between fibroblasts and the microenvironment is crucial for developing targeted therapeutic interventions aimed at modulating fibroblast activity and improving clinical outcomes in patients with pathological scars. Further research into the molecular pathways governing fibroblast behavior and their heterogeneity holds promise for advancing scar management strategies. This narrative review was performed to shed light on the mechanisms behind scar formation, with a special focus on the role of fibroblasts in the formation of different types of scars, providing insights into the pathophysiology of these conditions. Through the analysis of current knowledge, this review seeks to identify the key cellular and molecular mechanisms involved in fibroblast activation, collagen synthesis, and extracellular matrix remodeling in hypertrophic scar, keloid, or atrophic scar formation. [ABSTRACT FROM AUTHOR]

Background: Microvascular thrombosis following free tissue transfer presents a complex challenge for surgeons and carries the potential risk of flap failure. The application of fibrinolytic agents represents a robust therapeutic option. The aim of this systematic review is to provide a comprehensive overview of the clinical use of fibrinolytic drugs in the rescue of compromised free flaps. Methods: A systematic literature search for clinical studies detailing the utilization of fibrinolytic agents for salvaging free flaps was conducted using the PubMed and Web of Science databases. The inclusion criteria encompassed English-language publications that specifically addressed the clinical application of fibrinolytic agents for free-flap salvage. Results: A total of 331 articles were screened after excluding duplicates, with 56 meeting the inclusion criteria. Among these, 21 were clinical trials (evidence level III), and 35 were case studies (evidence level IV/V). In total, 459 flaps underwent treatment with fibrinolytic agents. Conclusion: The application of fibrinolytic agents appears to be a valuable intervention for rescuing compromised free flaps attributable to microvascular compromise. Notably, no prospective randomized trials have been published on this subject, and the evidence within the existing literature is characterized by its limited and heterogeneous nature. Further research is imperative to gather data on the efficacy, dosage, and safety profile of fibrinolytic agents. [ABSTRACT FROM AUTHOR]

OBJECTIVES Open in new tab Download slide Open in new tab Download slide The anatomical distribution pattern of epidural intraspinal arteries is not entirely understood but is likely to substantially impact maintaining perfusion during segmental artery sacrifice when treating acute and chronic thoraco-abdominal aortic diseases. We investigated the anatomical distribution pattern of intraspinal arteries. METHODS Twenty fresh, non-embalmed cadaveric human bodies were studied. Anatomical dissection and investigation of the epidural arterial network were performed according to a standardized protocol. We used a generalized mixed linear model to test whether the presence probability for certain vessels differed between vertebrae/segments. RESULTS There was craniocaudal continuity of all ipsilateral longitudinal connections from T1 to L5 by the anterior radicular artery. The mean [±standard deviation (SD)] number of transverse anastomoses was 9.7 ± 2.1. The presence probability of transverse anastomoses along the spine was different between vertebrae (P  < 0.0001). There were 2 distribution peaks along the spine: 1 peak around T4–T6 and 1 around T11. The mean (±SD) number of thoracic and lumbar anterior radiculomedullary arteries (ARMAs) was 3.0 ± 1.1. The probability of the presence of ARMAs along the spine was different for each vertebral segment (P  < 0.0001). Between ARMAs there were gaps of up to a maximum of 9 vertebrae. All Adamkiewicz arteries were located caudally to T7. The median segment of the Adamkiewicz presence was T10/11. CONCLUSIONS The epidural collateral network shows craniocaudal continuity. The number of transverse anastomoses is high. The number of ARMAs is low, and there is considerable variation in their distribution and offspring, which is highly likely to impact perfusion during segmental artery sacrifice when treating thoraco-abdominal aortic disease. [ABSTRACT FROM AUTHOR]