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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
Fibrogenic cytokines and extent of fibrosis in muscle of dogs with X-linked golden retriever muscular dystrophy
Laura Passerini,Pia Bernasconi,Fulvio Baggi,Paolo Confalonieri,Francesca Cozzi,Ferdinando Cornelio,Renato Mantegazza +6 more
TL;DR: The hypothesis that cytokines are actively involved in fibrosis in golden retriever muscular dystrophy, as it seems to be in humans, is sustained and the utility of this model for investigating new therapeutic approaches for Duchenne dystrohy is confirmed.
Journal ArticleDOI
Apoptosis of macrophages during the resulution of muscle inflammation.
TL;DR: The time course of apoptosis and concentration of apoptotic cells within damaged muscle fibers indicates that apoptosis contributes to returning ED1+ cells to control concentration during the resolution of inflammation, however, apoptosis of ED2+ cells during the first week following injury is not sufficient to return ED2- cell concentrations to control values.
Journal ArticleDOI
Impaired recovery of dysferlin-null skeletal muscle after contraction-induced injury in vivo.
TL;DR: It is reported that dysferlin-null muscles produce higher contractile torque, and are equally susceptible to initial injury but recover from injury more slowly, while recovery of control muscles from injury primarily involves sarcolemmal repair whereas recovery of dysferlins- null muscles primarily involves myogenesis without repair and long-term survival of myofibers.
Journal ArticleDOI
A quantitative study of the muscle satellite cells in various neuromuscular disorders.
TL;DR: The regenerative ability of muscles was studied in various neuromuscular disorders by quantitative electron microscopy using two indices of both the satellite cell population and the euchromatin percentage, which suggest that some defects of satellite cell function probably exist in progressive muscular dystrophy and amyotrophic lateral sclerosis, while in polymyositis the muscle fiber may have the ability to regenerate completely.
Journal ArticleDOI
Chemotactic behavior of myoblasts
TL;DR: It is shown here, for the first time, that embryonic skeletal muscle cells have the capacity to migrate toward a gradient of platelet-derived growth factor (PDGF) and PDGF-like factors present in serum and chick embryo extract (CEE).