| O-linked beta-n-acetylglucosamine (O-GlcNAc) glycosylation is an important reversible and dynamic post-translational modification. Through the dynamic regulation of O-GlcNAc transferase (OGT) and O-GlcNAc enzyme (OGA), various cellular processes are affected. In recent years, with the deepening of research, it has been found that it plays an important role in muscle and bone metabolic diseases, participates in maintaining musculoskeletal homeostasis, and regulates the occurrence and development of musculoskeletal decay diseases. Therefore, this paper summarizes the mechanism of O-GlcNAc glycosylation in musculoskeletal decay diseases, and explores its role in promoting bone formation, regulating the expression of osteogenic markers, and maintaining bone homeostasis through Wnt/β-catenin pathway and Ca2+-PKA-Gfat1 axis during bone remodeling. O-GlcNAc glycosylation promotes osteoclast differentiation in the early stage, affects oxidative phosphorylation and cell-cell fusion through RANKL/TNF-α,NF-κB pathway, inhibits osteoclast generation, thereby reducing bone resorption. In terms of muscle regeneration, O-GlcNAc glycosylation regulates the expression of Mef2c and Myogenin, promotes the differentiation of myoblasts and the formation of multi-nuclear muscle fibers, maintains the health and function of satellite cells, and promotes the mechanism of muscle repair and regeneration. The problems existing in the current research are summarized and prospected, in order to provide new ideas for clinical prevention and treatment of sarcopenia - osteoporosis. |