RESUMEN
The clinical treatment of joint contracture due to immobilization remains difficult. The pathological changes of muscle tissue caused by immobilization-induced joint contracture include disuse skeletal muscle atrophy and skeletal muscle tissue fibrosis. The proteolytic pathways involved in disuse muscle atrophy include the ubiquitin-proteasome-dependent pathway, caspase system pathway, matrix metalloproteinase pathway, Ca-dependent pathway and autophagy-lysosomal pathway. The important biological processes involved in skeletal muscle fibrosis include intermuscular connective tissue thickening caused by transforming growth factor-β1 and an anaerobic environment within the skeletal muscle leading to the induction of hypoxia-inducible factor-1α. This article reviews the progress made in understanding the pathological processes involved in immobilization-induced muscle contracture and the currently available treatments. Understanding the mechanisms involved in immobilization-induced contracture of muscle tissue should facilitate the development of more effective treatment measures for the different mechanisms in the future.
Asunto(s)
Humanos , Atrofia , Autofagia , Calcio , Metabolismo , Caspasas , Metabolismo , Tejido Conectivo , Metabolismo , Patología , Contractura , Metabolismo , Patología , Terapéutica , Fibrosis , Inmovilización , Articulaciones , Lisosomas , Metabolismo , Metaloproteinasas de la Matriz , Metabolismo , Músculo Esquelético , Metabolismo , Patología , Complejo de la Endopetidasa Proteasomal , Metabolismo , Proteolisis , Transducción de Señal , Fisiología , Factor de Crecimiento Transformador beta1 , Metabolismo , Ubiquitina , MetabolismoRESUMEN
@#Skeletal muscle has high regenerative capability. It is able to regenerate completely after acute traumatic damage, while the repairing process often accompanied by fibrosis in the chronic degenerative conditions such as muscular dystrophy and repeated muscle fiber damage. Through in-depth study on the mechanisms of skeletal muscle fibrosis in the past decade, it has been found that a variety of cells and regulatory molecules involved in the process, especially muscle satellite cells-derived myofibroblasts, transforming growth factor β (TGF-β) and other fibrosis promoting growth factors. This review focused on the cellular and molecular mechanisms of the skeletal muscle fibrosis and relevant antagonistic strategies.