{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,15]],"date-time":"2026-03-15T07:02:16Z","timestamp":1773558136742,"version":"3.50.1"},"reference-count":44,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T00:00:00Z","timestamp":1761523200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T00:00:00Z","timestamp":1761523200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82370983, X.D.W."],"award-info":[{"award-number":["82370983, X.D.W."]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81900984, J.N.Z."],"award-info":[{"award-number":["81900984, J.N.Z."]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oral Diseases"],"published-print":{"date-parts":[[2025,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Elucidate the mechanism underlying chondrocyte apoptosis induced by abnormal glycometabolism in the early stages of temporomandibular joint osteoarthritis (TMJOA) and identify potential therapeutic targets.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Design<\/jats:title>\n                    <jats:p>Established TMJOA model by monosodium iodoacetate(MIA), a direct inhibitor of glyceraldehyde 3\u2010phosphate dehydrogenase(GAPDH). Assessed the relationship between chondrocyte apoptosis and the levels of advanced glycation end products (AGEs) and their receptor (RAGE). Confirmed the apoptosis\u2010inhibitory effect of AGEs by RAGE inhibitor FPS\u2010ZM1. Verified the role of p38 in the up\u2010regulation of cleaved caspase\u20103. Investigated the effect of glyceraldehyde 3\u2010phosphate (G3P) in AGEs\u2010RAGE pathway. verified the universality of the AGEs\u2010RAGE pathway in occlusal interference\u2010induced TMJOA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In the early stages of TMJOA, chondrocyte apoptosis was associated with an upregulation of AGEs and RAGE. AGEs induced chondrocyte apoptosis by activating p38 through a RAGE\u2010dependent pathway. Inhibition of GAPDH led to the accumulation of G3P, resulting in an upregulation of AGEs and RAGE. Inhibition of RAGE reversed chondrocyte apoptosis following GAPDH inhibition. Local joint injection of FPS\u2010ZM1 alleviated TMJOA induced by both MIA and OI.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Altered glycometabolism can induce chondrocyte apoptosis through the AGEs\u2010RAGE axis, suggesting that RAGE may serve as a therapeutic target for TMJOA.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/odi.70011","type":"journal-article","created":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T05:02:27Z","timestamp":1761627747000},"page":"3395-3407","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Disturbed Glycometabolism\u2010Induced Chondrocyte Apoptosis Contributes to TMJOA"],"prefix":"10.1111","volume":"31","author":[{"given":"Yidan","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Orthodontics Peking University School and 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