Volume 4,Issue 4
As a representative degenerative joint disease, the pathological mechanism of osteoarthritis has increasingly highlighted the critical role of SIRT3 protein in various bone-related disorders. Beyond its significant impact on osteoarthritis, mitochondrial dysfunction is closely linked to the pathogenesis of multiple bone diseases, including osteoporosis, osteonecrosis, bone erosion in rheumatoid arthritis, abnormal fracture healing, and bone tumors. This review systematically explores how SIRT3 regulates mitochondrial function, thereby influencing metabolic processes, apoptosis, autophagy, and senescence in various bone-related cells such as osteoblasts, osteoclasts, osteocytes, and chondrocytes. By conducting cross-disease comparative analysis, we reveal the central role of the SIRT3-mitochondrial function axis in maintaining skeletal homeostasis, providing important theoretical basis and research directions for the future development of broad-spectrum skeletal protection strategies targeting SIRT3.