{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T01:45:34Z","timestamp":1791769534258,"version":"4.3.4"},"reference-count":130,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,10,11]],"date-time":"2026-10-11T00:00:00Z","timestamp":1791676800000},"content-version":"vor","delay-in-days":10,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Diabetes"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\u03b2\u2010cell dedifferentiation in humans is considered as a mechanism underlying \u03b2\u2010cell failure, which is characterized by the loss of their differentiated identity and reversion to a fetal\u2010like state. In humans, significant increases in the hormones\u2010negative\/Chromogranin A\u2010positive endocrine cells were detected in islets from T2D individuals, which were accompanied by decreased expressions of the \u03b2\u2010cell identity transcription factors (NKX6.1, MAFA, etc.) and reactivation of the progenitor marker, NEUROGENIN 3, and dramatic inductions of the dedifferentiation marker, ALDH1A3 and BACH2. The observation of increased dysfunctional dedifferentiated \u03b2\u2010cells in non\u2010diabetic patients with chronic pancreatitis or pancreatic ductal adenocarcinoma as well as in non\u2010diabetic aged subjects proposed that \u03b2\u2010cell dedifferentiation is not only a major mechanism of pancreatogenic diabetes and age\u2010related diabetes but also an initial trigger for human \u03b2\u2010cell failure before hyperglycemia occurs. Indeed, the finding that the ratio of dedifferentiated \u03b2\u2010cells is inversely related to HOMA\u2010\u03b2 and 2h\u2010C Peptide in subjects without a diabetes history further supports the contribution of \u03b2\u2010cell dedifferentiation to \u03b2\u2010cell failure in humans. Considerable efforts have been made and are still required to identify targets and pathways (in)dependent of hyperglycemia that trigger dedifferentiation in human \u03b2\u2010cells. These findings hold promise for the development of effective therapeutic strategies aimed at preventing or reversing this process, thereby maintaining or restoring functional \u03b2\u2010cell mass.<\/jats:p>","DOI":"10.1111\/1753-0407.70280","type":"journal-article","created":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T01:35:59Z","timestamp":1791768959000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Human \u03b2\u2010Cell Dedifferentiation and Diabetes"],"prefix":"10.1111","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-5192-7323","authenticated-orcid":false,"given":"Jiajun","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Endocrine and Metabolic Diseases Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine  Shanghai China"},{"name":"National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission Shanghai Key Laboratory for Endocrine Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinsook","family":"Son","sequence":"additional","affiliation":[{"name":"Weill Center for Metabolic Health, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine Weill Cornell Medicine  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0664-7502","authenticated-orcid":false,"given":"Qidi","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Endocrine and Metabolic Diseases Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine  Shanghai China"},{"name":"National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission Shanghai Key Laboratory for Endocrine Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine  Shanghai China"},{"name":"Sino\u2010French Research Center for Life Sciences and Genomics Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,10,11]]},"reference":[{"key":"e_1_2_13_2_1","doi-asserted-by":"crossref","first-page":"92","DOI":"10.1111\/nyas.12031","article-title":"Islet Beta Cell Mass in Diabetes and How It Relates to Function, Birth, and Death","volume":"1281","author":"Weir G. 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