| Mitophagy, crucial for cell quality control, is vital for muscle and bone health. This review explores its molecular mechanisms in sarcopenia (SP) and osteoporosis (OP), focusing on BNIP3, the PINK1-Parkin pathway, the AMPK/ULK1 axis, and Sirtuins family. These pathways maintain muscle and bone function by removing damaged mitochondria, stabilizing energy metabolism, and reducing oxidative stress. In osteosarcopenia (OS), mitophagy disruption may hasten muscle and bone degeneration and increase fracture risks. While mitophagy's role in SP and OP is established, its function in OS remains largely unexplored. Future research should delve into mitophagy's specific mechanisms in OS, particularly its regulatory role in muscle-bone interactions. Developing mitophagy-targeted interventions, like pharmacological or gene therapies to enhance mitophagy activity, could open new treatment avenues for SP, OP, and OS. Integrating multi-omics and animal models to study mitophagy's molecular networks and dynamic regulation in the musculoskeletal system may reveal these diseases' pathological bases, offering solid theoretical grounds for clinical therapy. In summary, the study of mitophagy, central to muscle and bone health, may deepen our understanding of SP, OP, and OS pathogenesis and provide clues for innovative treatments. |