Journal of Clinical Medicine, Journal Year: 2024, Volume and Issue: 13(22), P. 6641 - 6641

Published: Nov. 5, 2024

Rotator cuff calcific tendinopathy and arthrofibrosis of the shoulder (adhesive capsulitis) are debilitating musculoskeletal disorders that significantly impact joint function impair quality life. Despite its high prevalence common clinical presentation, metabolic mechanisms underlying these conditions characterized by pain, reduced mobility, remain poorly understood. This review aims to elucidate role processes implicated in pathogenesis arthrofibrosis. We will be focusing on mechanistic how contribute disease progression can direct potential therapeutic targets. Calcific is marked aberrant calcium deposition within tendons, influenced disrupted phosphate homeostasis, altered cellular responses. Key molecular pathways, including bone morphogenetic proteins (BMPs), Wnt signaling, transforming growth factor-beta (TGF-β), play crucial roles pathophysiology calcification, imbalance, muscle fibrosis. In contrast, involves excessive collagen fibrosis capsule, driven dysregulation inflammation. The TGF-β signaling pathway inflammatory cytokines, such as interleukin-6 (IL-6), central fibrotic response. A comparative analysis reveals both shared distinct pathways between conditions, highlighting interplay inflammation, metabolism, extracellular matrix remodeling, deposition, migration glenohumeral joints, resulting adhesive capsulitis, thereby providing insights into their pathophysiology. discusses current approaches limitations, advocating for development targeted therapies address specific dysregulations. Future strategies focus developing interventions dysregulation, aiming improve patient outcomes advance management. offers a comprehensive overview involved arthrofibrosis, foundation future research development.

Language: Английский