The role of TGF‐β1 during skeletal muscle regeneration

Abstract

The injury of adult skeletal muscle initiates series of well-coordinated events that lead to the efficient repair of the damaged tissue. Any disturbances during muscle myolysis or reconstruction may result in the unsuccessful regeneration, characterised by strong inflammatory response and formation of connective tissue, that is, fibrosis. The switch between proper regeneration of skeletal muscle and development of fibrosis is controlled by various factors. Amongst them are those belonging to the transforming growth factor b family. One of the TGF-b family members is TGF-b1, a multifunctional cytokine involved in the regulation of muscle repair via satellite cells activation, connective tissue formation, as well as regulation of the immune response intensity. Here, we present the role of TGF-b1 in myogenic differentiation and muscle repair. The understanding of the mechanisms controlling these processes can contribute to the better understanding of skeletal muscle atrophy and diseases which consequence is fibrosis disrupting muscle function.

Neutralization of transforming growth factor (TGF)-β1 activity reduced fibrosis and enhanced regeneration of glycerol-injured rat muscle

“…Van Linthout et al [25] reported that TGF-β1 stimulates fibroblast proliferation to produce ECM proteins. Decreased fibroblast migration and diminished ECM production at the injury site reduces fibrosis and enhances muscle repair [3]. Taken together, our results and those of the previous studies suggest that blockage of TGF-β1 activity by a neutralizing antibody reduces muscle fibrosis.…”

Skeletal Muscle Immunometabolism in Women With Polycystic Ovary Syndrome: A Meta-Analysis

“…Fibrosis in skeletal muscle can impair muscle function and affect muscle fiber regeneration after injury (Delaney et al, 2017;Mahdy, 2019). Tissue fibrosis is often initiated and maintained through TGF-beta signaling and has been suggested to be associated with insulin resistance and steatosis in PCOS (Petta et al, 2017;Stepto et al, 2019).…”

miR-24 and miR-122 Negatively Regulate the Transforming Growth Factor-β/Smad Signaling Pathway in Skeletal Muscle Fibrosis

“…Myofibroblast, the initiator of fibrotic process, is acknowledged to be derived from different cell lines, including inflammatory cells, fibro/adipogenic progenitors, and fibroblasts. 15 Transforming growth factor-β (TGF-β), 16 connective tissue growth factor (CTGF), and platelet-derived growth factor (PDGF) families have been identified to play a role in this pathology, among which TGF-β, a strong profibrotic cytokine, can stimulate the synthesis of ECM, and then result in skeletal muscle fibrosis. As the canonical TGF-β pathway, TGF-β/Smad pathway plays a pivotal role in mediating the fibrotic process, 17 and modalities against TGF-β-related pathways have been proven to potentially alleviate the pathology.…”