{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T21:11:00Z","timestamp":1793913060004,"version":"4.8.0"},"reference-count":216,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,9,5]],"date-time":"2025-09-05T00:00:00Z","timestamp":1757030400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Endocrinol."],"abstract":"<jats:p>Diabetic patients have a higher tendency for vascular calcification (VC). This indicates a possible link between abnormal glucose metabolism and the development of VC. High glucose levels are a major cause of vascular calcification in diabetic patients. Vascular smooth muscle cells (VSMCs) are important functional units of the arterial media and show heterogeneity. Sustained hyperglycemia drives VSMCs to undergo a phenotypic transition from contractile state to osteo-\/chondrogenic lineages through multiple pathophysiological mechanisms. Specifically, hyperglycemia stimulates metabolic reprogramming. This includes enhancing advanced glycation end products (AGEs), activating the diacylglycerol-dependent protein kinase C (PKC) pathway, disrupting the pentose phosphate flux (PPP), and dysregulating the hexosamine biosynthesis pathway (HBP). These changes trigger vesicles-mediated mineralization (including matrix\/extracellular vesicles), oxidative stress, inflammatory cascades, and an imbalance between autophagy and apoptosis. This review systematically describes the metabolic remodelling induced by high glucose and its regulatory mechanisms in vascular calcification.<\/jats:p>","DOI":"10.3389\/fendo.2025.1589160","type":"journal-article","created":{"date-parts":[[2025,9,5]],"date-time":"2025-09-05T11:38:35Z","timestamp":1757072315000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Regulation of osteogenic differentiation in vascular smooth muscle cells under high-glucose condition"],"prefix":"10.3389","volume":"16","author":[{"given":"Jingjing","family":"Guo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laijing","family":"Du","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2025,9,5]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.diabres.2015.05.037","article-title":"Update of mortality attributable to diabetes for the IDF Diabetes Atlas: Estimates for the year 2013","volume":"109","year":"2015","journal-title":"Diabetes Res Clin Pract"},{"key":"B2","doi-asserted-by":"publisher","first-page":"107843","DOI":"10.1016\/j.diabres.2019.107843","article-title":"Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9(th) edition","volume":"157","author":"Saeedi","year":"2019","journal-title":"Diabetes Res Clin Pract"},{"key":"B3","doi-asserted-by":"publisher","first-page":"4461311","DOI":"10.1155\/2021\/4461311","article-title":"Epidemiological research advances in vascular calcification in diabetes","volume":"2021","author":"Yao","year":"2021","journal-title":"J Diabetes Res"},{"key":"B4","doi-asserted-by":"publisher","first-page":"259","DOI":"10.1186\/s12933-024-02318-8","article-title":"Association of diabetes with cardiovascular calcification and all-cause mortality in end-stage renal disease in the early stages of hemodialysis: a retrospective cohort study","volume":"23","author":"Li","year":"2024","journal-title":"Cardiovasc Diabetol"},{"key":"B5","doi-asserted-by":"publisher","first-page":"58","DOI":"10.1186\/s10020-024-00817-8","article-title":"Glucagon-like peptide-1 receptor agonist exendin 4 ameliorates diabetes-associated vascular calcification by regulating mitophagy through the AMPK signaling pathway","volume":"30","author":"Chen","year":"2024","journal-title":"Mol Med"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.3390\/ijms21082685","article-title":"Vascular calcification-new insights into its mechanism","volume":"21","author":"Lee","year":"2020","journal-title":"Int J Mol Sci"},{"key":"B7","doi-asserted-by":"publisher","first-page":"13730","DOI":"10.1038\/s41598-018-31877-6","article-title":"Advanced glycation end products accelerate calcification in VSMCs through HIF-1\u03b1\/PDK4 activation and suppress glucose metabolism","volume":"8","author":"Zhu","year":"2018","journal-title":"Sci Rep"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.3109\/00365518909089084","article-title":"Quantification of fibronectin in extracts of human aortae by an ELISA","volume":"49","author":"Rasmussen","year":"1989","journal-title":"Scand J Clin Lab Invest"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1159\/000226225","article-title":"Advanced glycation end products induce calcification of vascular smooth muscle cells through RAGE\/p38 MAPK","volume":"46","author":"Tanikawa","year":"2009","journal-title":"J Vasc Res"},{"key":"B10","doi-asserted-by":"publisher","first-page":"104861","DOI":"10.1016\/j.phrs.2020.104861","article-title":"Diabetes and calcification: The potential role of anti-diabetic drugs on vascular calcification regression","volume":"158","author":"Ghosh","year":"2020","journal-title":"Pharmacol Res"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2000.tb06338.x","article-title":"Enhanced expression of osteopontin by high glucose. 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