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O\u2010GlcNAcylation is a dynamic and reversible posttranslational modification where uridine diphosphate N\u2010acetylglucosamine (UDP\u2010GlcNAc) is added or removed from serine\/threonine residues of proteins by OGT and OGA, respectively. Emerging evidence indicates that appropriate O\u2010GlcNAcylation is essential for bone remodeling, although its specific effects remain controversial.<\/jats:p><\/jats:sec><jats:sec><jats:title>Aims<\/jats:title><jats:p>This review aims to summarize the process of O\u2010GlcNAcylation and critically evaluate its specific effects on osteoblast\u2010mediated and osteoclast\u2010mediated bone remodeling.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials &amp; Methods<\/jats:title><jats:p>Based on a comprehensive analysis of published scientific literature, we synthesized the current evidence regarding the role of O\u2010GlcNAcylation in bone cell differentiation and function, and its association with osteoporosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Our analysis reveals that cellular demands for O\u2010GlcNAcylation vary during osteoblastic and osteoclastic differentiation. Moderate O\u2010GlcNAcylation is essential for osteoblast differentiation, whereas dynamic alterations in O\u2010GlcNAcylation are crucial for osteoclast differentiation. Furthermore, elevated O\u2010GlcNAcylation levels are consistently observed in both primary and secondary osteoporosis cases, suggesting a potential pathogenic role in the dysregulation of bone remodeling.<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p>These findings indicate that the effects of O\u2010GlcNAcylation are cell type\u2010 and differentiation stage\u2010dependent in bone. The observed elevation of O\u2010GlcNAcylation in osteoporosis underscores its potential contribution to the dysregulation of bone remodeling pathways.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>This review provides novel mechanistic insights into osteoporosis pathogenesis via dysregulation of the O\u2010GlcNAcylation post\u2010translational modification. Understanding these mechanisms will facilitate the development of novel therapeutic strategies targeting O\u2010GlcNAcylation to restore balanced bone remodeling.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.70080","type":"journal-article","created":{"date-parts":[[2025,7,17]],"date-time":"2025-07-17T05:01:01Z","timestamp":1752728461000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Emerging Roles of Protein O\u2010<scp>GlcNAcylation<\/scp> in Bone Remodeling: New Insights Into Osteoporosis"],"prefix":"10.1111","volume":"241","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4379-7403","authenticated-orcid":false,"given":"Jinpeng","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Orthopedics First Hospital of China Medical University  Shenyang 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