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Skeletal muscle regeneration is a complex biological process that restores damaged muscle tissue through the activation of myogenic stem cells, primarily satellite cells (Yin et al., 2013, Physiol Rev). Upon injury, these quiescent cells are activated, proliferate as myoblasts, and eventually differentiate and fuse to form new myofibers or repair existing ones, a process orchestrated by myogenic regulatory factors such as MyoD and Myogenin (Zammit, 2017, J Cell Sci). This pathway is critically involved in the pathogenesis of Muscular Dystrophies and age-related Sarcopenia, where the regenerative capacity is exhausted or inhibited (Dumont et al., 2015, Annu Rev Cell Dev Biol). Therapeutic strategies often focus on inhibiting negative regulators like myostatin or enhancing growth factors like IGF-1 to promote muscle mass and function (Rybalka et al., 2020, Cells). However, pharmacological manipulation of these pathways requires careful management to avoid systemic side effects, such as unintended cellular proliferation or metabolic disturbances (Tidball, 2017, Nat Rev Immunology).
Modulation of myogenic regulatory factors, inhibition of the myostatin/activin signaling pathway, and activation of the IGF-1/Akt/mTOR hypertrophic signaling axis to promote satellite cell proliferation and differentiation.
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