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Skeletal myofiber regeneration refers to the process by which skeletal muscle fibers are repaired or replaced following injury, disease, or normal turnover. This regenerative process relies primarily on muscle stem cells, called satellite cells, which become activated upon injury, then proliferate, differentiate into myoblasts, and fuse to form new or repair existing myofibers[1][5][6][7]. Key transcription factors marking these stages include Pax7, MYF5, MyoD, and myogenin. The regeneration process is tightly regulated by numerous cell-cell interactions (e.g., between satellite cells, immune cells, fibroblasts) and by signaling molecules such as IGF-1, FGF, HGF, PDGF, LIF, TNF-α, IL-6, and TGF-β[1][2]. Failure or disruption of these mechanisms is implicated in a diverse range of muscle diseases, from muscular dystrophies to age-related muscle decline[6]. This entity is a biological process rather than a single molecule, receptor, enzyme, or canonical therapeutic target. For structured drug discovery purposes, focus should be shifted to individual molecules or pathways essential for this process—such as Pax7, MYF5, MyoD, IGF-1 receptor, or TGF-β signaling.
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