{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T16:58:46Z","timestamp":1786121926734,"version":"build-2736575974"},"reference-count":57,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,4,20]],"date-time":"2026-04-20T00:00:00Z","timestamp":1776643200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,4,20]],"date-time":"2026-04-20T00:00:00Z","timestamp":1776643200000},"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":["52263014"],"award-info":[{"award-number":["52263014"]}],"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":["82060775"],"award-info":[{"award-number":["82060775"]}],"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":["82260827"],"award-info":[{"award-number":["82260827"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["dom-pubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2026,7]]},"abstract":"ABSTRACT<\/jats:title>\n \n Background and Objective<\/jats:title>\n \n Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterised by insulin resistance and \u03b2\u2010cell impairment. Dedifferentiation of pancreatic \u03b2\u2010cells contributes to the progression of T2DM, influencing insulin secretion through mechanisms such as mitochondrial dysfunction, Ca\n 2+<\/jats:sup>\n overload and impaired autophagy. This study investigated the effects of terpinen\u20104\u2010ol (T4O) on \u03b2\u2010cell dedifferentiation and mitochondrial autophagy, with an emphasis on the role of the Parkin\/MCU signalling pathway.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n A T2DM mouse model was generated using a high\u2010fat diet (HFD, 60% fat) and STZ (50\u2009mg\/kg) injection, and \u03b2\u2010cell dedifferentiation was induced by high glucose (HG) treatment in MIN6 cells. T4O was administered, and its effects on mitochondrial autophagy and \u03b2\u2010cell dedifferentiation were evaluated. The mitochondrial autophagy agonist NMN and the MCU inhibitor RU360 were used to assess the interplay between mitophagy and Ca\n 2+<\/jats:sup>\n signalling. Parkin was overexpressed in\u00a0vitro and in\u00a0vivo to determine its contribution to mitochondrial autophagy and Ca\n 2+<\/jats:sup>\n regulation. The investigation of the mechanism of the Parkin\/MCU signalling pathway involved co\u2010immunoprecipitation (Co\u2010IP), mass spectrometry (MS) and protein synthesis inhibition assays.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n T4O improved blood glucose levels and insulin resistance in diabetic mice. In\u00a0vitro and in\u00a0vivo, T4O reduced the expression of dedifferentiation markers (such as OCT4, MafA and Pdx1 and Ngn3), increased the expression of mitochondrial autophagy\u2010related proteins (PINK1, Parkin, Beclin and LC3\u2010II\/I) and modulated the expression of MCU and Drp1 (downregulated) as well as MFN2 (upregulated). T4O also alleviated HG\u2010induced mitochondrial damage, including ultrastructural abnormalities, decreased membrane potential, elevated reactive oxygen species and Ca\n 2+<\/jats:sup>\n overload. In addition, preincubation of MIN6 cells with T4O or the mitochondrial autophagy agonist NMN can reduce HG\u2010induced mitochondrial Ca\n 2+<\/jats:sup>\n overload, promote mitochondrial autophagy, reduce MCU protein levels and inhibit pancreatic \u03b2\u2010cell dedifferentiation. Similar results were observed when Parkin was overexpressed both in\u00a0vivo and in\u00a0vitro. Moreover, the opposite results were obtained in Parkin\u2010knockdown MIN6 cells. Mechanistically, T4O facilitated Parkin\u2010mediated MCU ubiquitination degradation by interacting with MCU at lysine residue K320; notably, mutation of K320 to arginine (K320R) abolished T4O\u2010induced MCU ubiquitination and reversed the protective effects against \u03b2\u2010cell dedifferentiation. These findings indicate that T4O increases Parkin expression, increases MCU ubiquitination and reduces mitochondrial Ca\n 2+<\/jats:sup>\n accumulation, thereby protecting against T2DM\u2010induced \u03b2\u2010cell dedifferentiation.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n \n T4O enhances Parkin expression and targets the K320 site of MCU to promote Parkin\u2010mediated, ubiquitination\u2010mediated degradation of MCU, thereby alleviating mitochondrial calcium overload and mitophagy and consequently inhibiting the transdifferentiation of pancreatic islet \u03b2\u2010cells in diabetes. These data support T4O as a potential therapeutic candidate for T2DM by targeting mitochondrial Ca\n 2+<\/jats:sup>\n signalling and autophagy.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/dom.70774","type":"journal-article","created":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T05:23:42Z","timestamp":1776749022000},"page":"5871-5892","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Mechanism of\n Terpinen\u20104\u2010ol<\/scp>\n in Suppressing \u03b2\u2010Cell Dedifferentiation: Restoring Mitophagy and Alleviating Mitochondrial Calcium Overload via Parkin\u2010Mediated\n MCU<\/scp>\n Degradation"],"prefix":"10.1111","volume":"28","author":[{"given":"Yanyan","family":"Zhang","sequence":"first","affiliation":[{"name":"State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine Guizhou Medical University Guian New District Guizhou China"},{"name":"The 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District Guizhou China"},{"name":"Guizhou International Science & Technology Cooperation Base for Druggability Research of Natural Medicines Guizhou Medical University Guian New District Guizhou China"},{"name":"Bijie Medical College Bijie Guizhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"He","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine Guizhou Medical University Guian New District Guizhou China"},{"name":"The High\u2010Efficacy Application of Natural Medicinal Resources Engineering Center of Guizhou Province, School of Pharmaceutical Sciences Guizhou Medical University Guian New District Guizhou China"},{"name":"Guizhou International Science & Technology Cooperation Base for Druggability Research of Natural Medicines Guizhou Medical University Guian New District Guizhou China"},{"name":"Department of Pharmacy Qianxi People's Hospital 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