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O\u2010GlcNAcylation, a dynamic post\u2010translational modification, is closely linked to cardiovascular diseases, including VC. However, the exact role and molecular mechanism of O\u2010GlcNAc signaling in abnormal mineral metabolism\u2010induced VC remain unclear. In the current study, we found that the levels of O\u2010GlcNAc transferase (OGT) and global protein O\u2010GlcNAcylation were significantly upregulated in the artery tissues of mouse calcification models and CKD patients with VC. To further delineate the in\u00a0vivo role of OGT in VC, we generated\n                    <jats:italic>Ogt<\/jats:italic>\n                    smooth muscle cell\u2010specific knockout mice and challenged them with 5\/6 nephrectomy (5\/6 Nx) or high\u2010dose vitamin D3 to induce VC. Deletion of\n                    <jats:italic>Ogt<\/jats:italic>\n                    in VSMCs led to alleviated VC in response to 5\/6 Nx or VD3. Moreover, elevated O\u2010GlcNAcylation, induced by Thiamet\u2010G, facilitated osteogenic transdifferentiation in VSMCs in response to phosphate, whereas OSMI\u20101, which reduces O\u2010GlcNAcylation, exhibited an opposite phenotypic effect. Mechanistically, O\u2010GlcNAc signaling enhanced the osteogenic conversion of VSMCs through regulation of canonical Wnt\/\u03b2\u2010catenin pathway. Indeed, \u03b2\u2010catenin was O\u2010GlcNAcylated by OGT and further increased its transcriptional activity in VSMCs. Furthermore, pharmacological activation of Wnt\/\u03b2\u2010catenin signaling largely reversed the diminished aortic calcification caused by\n                    <jats:italic>Ogt<\/jats:italic>\n                    ablation. Our findings demonstrate that smooth muscle O\u2010GlcNAc signaling plays an important role in regulating hyperphosphatemia\u2010induced VC and reveal that O\u2010GlcNAcylation of \u03b2\u2010catenin protein modulates its content and activity in VSMCs.\n                  <\/jats:p>","DOI":"10.1096\/fj.202401649rr","type":"journal-article","created":{"date-parts":[[2024,12,20]],"date-time":"2024-12-20T06:41:04Z","timestamp":1734676864000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["O\u2010GlcNAc transferase promotes vascular smooth muscle calcification through modulating Wnt\/\u03b2\u2010catenin signaling"],"prefix":"10.1096","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9393-7454","authenticated-orcid":false,"given":"Lin","family":"Xu","sequence":"first","affiliation":[{"name":"Xinxiang Key Laboratory of Metabolism and Integrative Physiology, School of Forensic Medicine Xinxiang Medical 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