Skeletal muscle injury repair is a complex biological process involving multiple cell types, molecular signals, and physiological processes. After muscle injury, the activation and proliferation of satellite cells are key steps in skeletal muscle repair, yet this process is finely regulated by immune cells, extracellular matrix remodeling, and various cytokines. Initially, the local inflammatory response following injury is mediated by immune cells such as macrophages and neutrophils, which secrete pro-repair factors and regulate the function of satellite cells, thereby providing the necessary microenvironment for muscle repair. Meanwhile, the infiltration of fibro-adipogenic progenitor cells at the injury site and their subsequent differentiation also play a critical role in regulating muscle repair and hypertrophic responses. Dynamic remodeling of the extracellular matrix not only supports muscle fiber regeneration but also plays an important role in maintaining muscle homeostasis and functional recovery. Angiogenesis in skeletal muscle repair is also crucial, especially in promoting the supply of oxygen and nutrients to the repair site. With the development of molecular biology techniques, such as gene editing, stem cell transplantation, and tissue engineering, therapeutic strategies for skeletal muscle repair have been optimized. However, despite these advances, the mechanisms of novel molecules in skeletal muscle repair remain unclear and need further validation through in-depth clinical and basic research to assess their efficacy and safety. This review provides a comprehensive review of the latest research on the key biological mechanisms of skeletal muscle injury repair, focusing on the synergistic interaction of different cell types and signaling pathways, and discusses current challenges and future directions of research, aiming to provide new theoretical insights for clinical treatment of skeletal muscle injury.
Huang et al. (Fri,) studied this question.