Aberrant repair and fibrosis development in skeletal muscle

Abstract

The repair process of damaged tissue involves the coordinated activities of several cell types in response to local and systemic signals. Following acute tissue injury, infiltrating inflammatory cells and resident stem cells orchestrate their activities to restore tissue homeostasis. However, during chronic tissue damage, such as in muscular dystrophies, the inflammatory-cell infiltration and fibroblast activation persists, while the reparative capacity of stem cells (satellite cells) is attenuated. Abnormal dystrophic muscle repair and its end stage, fibrosis, represent the final common pathway of virtually all chronic neurodegenerative muscular diseases. As our understanding of the pathogenesis of muscle fibrosis has progressed, it has become evident that the muscle provides a useful model for the regulation of tissue repair by the local microenvironment, showing interplay among muscle-specific stem cells, inflammatory cells, fibroblasts and extracellular matrix components of the mammalian wound-healing response. This article reviews the emerging findings of the mechanisms that underlie normal versus aberrant muscle-tissue repair.

Structural Changes in the Skeletal Muscle Fiber of Adult Male Albino Rat Following Atorvastatin Treatment; the Possible Mechanisms of Atorvastatin Induced Myotoxicity

“…These findings might indicate the presence of regenerating fibers that usually appeared near areas of necrosis and degeneration [21]. After muscle injury, infiltrating inflammatory cells release cytokines and growth factors that might affect satellite cells leading to its activation and proliferation and finally to differentiation into myoblasts [22].…”

TGF-β Contributes to Impaired Exercise Response by Suppression of Mitochondrial Key Regulators in Skeletal Muscle

“…The recruitment of macrophages and neutrophils is often associated with acute eccentric or resistance exercise (30), but it can also occur after endurance exercise (31). TGF-b then activates fibroblasts in the muscle to produce extracellular matrix proteins and TGF-b itself (32), while muscle satellite cells and myofibers may contribute to the enhanced production of TGF-b and extracellular matrix proteins (33,34). This process possibly took place in all participants of our study after the first training sessions, as part of the normal regeneration program of an untrained muscle (32,35).…”

Histopathological changes in supraspinous ligaments, ligamentum flava and paraspinal muscle tissues of patients with ankylosing spondylitis

“…Abnormal dystrophic muscle repair and its end stage, fibrosis, are believed to represent the final common pathway of virtually all chronic neurodegenerative muscular diseases. 22 Therefore, such phenomena may generate pathological complications following AS occurrence.…”