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Chinese Journal of Traumatology ; (6): 93-98, 2019.
Article in English | WPRIM | ID: wpr-771633

ABSTRACT

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.


Subject(s)
Humans , Atrophy , Autophagy , Calcium , Metabolism , Caspases , Metabolism , Connective Tissue , Metabolism , Pathology , Contracture , Metabolism , Pathology , Therapeutics , Fibrosis , Immobilization , Joints , Lysosomes , Metabolism , Matrix Metalloproteinases , Metabolism , Muscle, Skeletal , Metabolism , Pathology , Proteasome Endopeptidase Complex , Metabolism , Proteolysis , Signal Transduction , Physiology , Transforming Growth Factor beta1 , Metabolism , Ubiquitin , Metabolism
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