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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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Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation
TL;DR: In this paper , small molecular selenoprotein K (SelK) plays crucial roles in the modulation of endoplasmic reticulum (ER) stress and against oxidative stress.
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Macrophages and regeneration: Lessons from the heart.
TL;DR: The present review aims to describe the latest discoveries about the possible role of macrophages in myocardial regeneration and discusses the promises and difficulties to translate the latest findings into new therapies.
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Lack of Heme Oxygenase-1 Induces Inflammatory Reaction and Proliferation of Muscle Satellite Cells after Cardiotoxin-Induced Skeletal Muscle Injury.
Magdalena Kozakowska,Katarzyna Pietraszek-Gremplewicz,Maciej Ciesla,Marta Seczynska,Iwona Bronisz-Budzyńska,Paulina Podkalicka,Karolina Bukowska-Strakova,Karolina Bukowska-Strakova,Agnieszka Loboda,Alicja Jozkowicz,Jozef Dulak +10 more
TL;DR: Heme oxygenase-1 modulates muscle repair mechanisms preventing its uncontrolled acceleration, and can be partially mimicked by stimulation of Hmox1+/+ SCs with monocyte chemoattractant protein-1,IL-6, IL-1β, and is associated with increased MyoD expression, suggesting that Hmx1-/- SCs are shifted toward more differentiated myogenic population.
Journal ArticleDOI
Proteomic profiling of mdx-4cv serum reveals highly elevated levels of the inflammation-induced plasma marker haptoglobin in muscular dystrophy.
Sandra Murphy,Paul Dowling,Margit Zweyer,Michael Henry,Paula Meleady,Rustam R. Mundegar,Dieter Swandulla,Kay Ohlendieck +7 more
TL;DR: Serum from the mdx-4cv model of Duchenne muscular dystrophy is characterized by the almost complete loss of the membrane cytoskeletal protein dystrophin, which triggers sarcolemmal instability, abnormal calcium homeostasis, increased proteolysis and impaired excitation-contraction coupling, and a serum component with greatly elevated levels was identified as the inflammation-inducible plasma marker haptoglobin.
Journal ArticleDOI
Matrix bound nanovesicle-associated IL-33 activates a pro-remodeling macrophage phenotype via a non-canonical, ST2-independent pathway.
George S. Hussey,Jenna L. Dziki,Yoojin C. Lee,Joseph G. Bartolacci,Marissa Behun,Heth R. Turnquist,Stephen F. Badylak +6 more
TL;DR: It is shown that IL-33 encapsulated within MBV bypass the classical IL33/ST2 receptor signaling pathway to direct macrophage differentiation into the reparative, pro-remodeling M2 phenotype, which in turn facilitates myogenesis of skeletal muscle progenitor cells.
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