The mechanisms and treatments of muscular pathological changes in immobilization-induced joint contracture: A literature review

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 2+ -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.

Preventive Effects of Dulaglutide on Disuse Muscle Atrophy Through Inhibition of Inflammation and Apoptosis by Induction of Hsp72 Expression

“…Muscle protein degradation is notably elevated in disused muscle and thought to involve the ubiquitin-proteasome-dependent pathway, caspase system pathway, and autophagy pathway (Wang et al, 2019). Of these, the ubiquitin-proteasome system (UPS) mediates the degradation of short-lived proteins and has been indicated as an important mechanism in disuse atrophy (Malavaki et al, 2015).…”

Effects of astaxanthin on the protection of muscle health (Review)

“…Hindlimb immobilization is another method to induce muscle atrophy. Immobilization refers to holding a joint or bone in place with a cast to prevent its movement, thus inducing muscle contracture and atrophy (35,36). In contrast, the rodents are in a head-down position to simulate weightlessness for hindlimb unloading (37).…”

Effect of Ultrashort Wave on Joint Dysfunction and Muscle Atrophy in a Rabbit Model of Extending Knee Joint Contracture: Enhanced Expression of MyoD

“…1 The normal ROM is difficult to restore once lost even through surgical treatment, and immobilization is a major cause of knee joint contracture. 2 Two different structural components which contained myogenic contracture and arthrogenic contracture make contribution to joint contracture formation. 3 Studies on animal muscles have shown that passive extensibility depends on the size and length of the muscle fibers and the amount and arrangement of connective tissue in the muscle belly.…”

“…Muscle atrophy is an important part of myogenic contracture. 2 Sustained muscle atrophy which caused by loss of tissue protein because of decreased synthesis and increased degradation, an increase in the amount of intramuscular connective tissue, and the arrangement of collagen fibrils in the endomysium severely affects the function of knee joint. 5 During the process of muscle atrophy from immobilization in shortened position, the mass of muscle was reduced.…”

“…6 Meanwhile, the length and cross-sectional area (CSA) of myofibers are contractible compared with normal. 2 MyoD is one of the earliest markers of myogenesis. 7 Recent evidence demonstrate that increasing ubiquitinproteasome-dependent proteolysis is closely related to muscle atrophy.…”