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Mechanisms of Muscle Injury, Repair, and Regeneration
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TLDR
The process of muscle injury, repair and regeneration that occurs in muscular dystrophy is used as an example of chronic muscle injury to highlight similarities and differences between the injury and repair processes that occur in acutely and chronically injured muscle.Abstract:
Skeletal muscle continuously adapts to changes in its mechanical environment through modifications in gene expression and protein stability that affect its physiological function and mass. However, mechanical stresses commonly exceed the parameters that induce adaptations, producing instead acute injury. Furthermore, the relatively superficial location of many muscles in the body leaves them further vulnerable to acute injuries by exposure to extreme temperatures, contusions, lacerations or toxins. In this article, the molecular, cellular, and mechanical factors that underlie muscle injury and the capacity of muscle to repair and regenerate are presented. Evidence shows that muscle injuries that are caused by eccentric contractions result from direct mechanical damage to myofibrils. However, muscle pathology following other acute injuries is largely attributable to damage to the muscle cell membrane. Many feaures in the injury-repair-regeneration cascade relate to the unregulated influx of calcium through membrane lesions, including: (i) activation of proteases and hydrolases that contribute muscle damage, (ii) activation of enzymes that drive the production of mitogens and motogens for muscle and immune cells involved in injury and repair, and (iii) enabling protein-protein interactions that promote membrane repair. Evidence is also presented to show that the myogenic program that is activated by acute muscle injury and the inflammatory process that follows are highly coordinated, with myeloid cells playing a central role in modulating repair and regeneration. The early-invading, proinflammatory M1 macrophages remove debris caused by injury and express Th1 cytokines that play key roles in regulating the proliferation, migration, and differentiation of satellite cells. The subsequent invasion by anti-inflammatory, M2 macrophages promotes tissue repair and attenuates inflammation. Although this system provides an effective mechanism for muscle repair and regeneration following acute injury, it is dysregulated in chronic injuries. In this article, the process of muscle injury, repair and regeneration that occurs in muscular dystrophy is used as an example of chronic muscle injury, to highlight similarities and differences between the injury and repair processes that occur in acutely and chronically injured muscle.read more
Citations
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References
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Journal ArticleDOI
Aging normal and dystrophic mouse muscle: analysis of myogenicity in cultures of living single fibers
TL;DR: There is no evidence that extensive myoblast proliferation in young dystrophic mice—and, by association, in Duchenne muscular dystrophy patients—depletes their myogenic responsiveness in later life when they become weak and wasted.
Journal ArticleDOI
Macrophage invasion does not contribute to muscle membrane injury during inflammation.
TL;DR: Muscle invasion by neutrophils is not sufficient to cause invasion by ED1+ macrophages and muscle membrane injury that occurs during reloading is independent of invasion byED1+ Macrophages.
Journal ArticleDOI
Changes in human skeletal muscle induced by long term eccentric exercise
TL;DR: It is concluded that muscular work of high tension can induce fine-structural alterations that results in a better stretchability of the muscle fibres, reduces the risk for mechanical damage and brings about an optimal overlap between actin and myosin filaments.
Journal ArticleDOI
Gross ultrastructural changes and necrotic fiber segments in elbow flexor muscles after maximal voluntary eccentric action in humans
TL;DR: It is demonstrated that the more severe end of the continuum of ultrastructural changes occurs in humans after voluntary exercise when maximal eccentric muscle actions are involved.
Journal ArticleDOI
The effect of muscle architecture on the biomechanical failure properties of skeletal muscle under passive extension
William E. Garrett,Pantelis K. Nikolaou,Beth M. Ribbeck,Richard R. Glisson,Anthony V. Seaber +4 more
TL;DR: It is demonstrated that all four muscle types tested show injury and rupture at the musculotendinous junction whether pulled from proximal or distal attach ment, regardless of muscle structure and rate of strain.