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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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Prednisolone decreases cellular adhesion molecules required for inflammatory cell infiltration in dystrophin-deficient skeletal muscle.
TL;DR: The data show that prednisolone is an effective anti-inflammatory in dystrophic muscle and may function by modulating CAM expression and reduce sarcolemmal damage and degeneration.
Journal ArticleDOI
Unexpected sarcolemmal complement membrane attack complex deposits on nonnecrotic muscle fibers in muscular dystrophies
Simone Spuler,Andrew G. Engel +1 more
TL;DR: The findings do not support a role for antibody-dependent complement-mediated muscle fiber injury in the major inflammatory muscle diseases.
Journal ArticleDOI
M1/70 attenuates blood-borne neutrophil oxidants, activation, and myofiber damage following stretch injury
TL;DR: Treatment with M1/70 attenuates neutrophil activation status, increases plasma IL-8 concentration, and minimizes myofiber damage 24 h postmuscle stretch injury indicate that CD11b-dependent respiratory burst is a major source of oxidants produced by the neutrophils.
Journal ArticleDOI
Matrix metalloproteinase-2 mediates stretch-induced activation of skeletal muscle satellite cells in a nitric oxide-dependent manner.
Michiko Yamada,Yoriko Sankoda,Ryuichi Tatsumi,Wataru Mizunoya,Yoshihide Ikeuchi,Kenji Sunagawa,Ronald E. Allen +6 more
TL;DR: Results from these experiments provide evidence that NO-activated MMP2 may cause release of HGF from the extracellular matrix of satellite cells and contribute to satellite cell activation.
Journal ArticleDOI
Tumor necrosis factor-alpha (TNF-alpha) stimulates chemotactic response in mouse myogenic cells.
Yvan Torrente,Elmostafa El Fahime,Nicolas Caron,R. Del Bo,Marzia Belicchi,Federica Pisati,Jacques P. Tremblay,Nereo Bresolin +7 more
TL;DR: It is proposed that TNF-α may promote myoblast migration directly through chemotactic activity and indirectly by enhancing MMP activity at the site of muscle injury.