{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T13:10:34Z","timestamp":1789477834794,"version":"build-2803163510"},"reference-count":62,"publisher":"SAGE Publications","issue":"10-12","license":[{"start":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T00:00:00Z","timestamp":1783641600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Beijing Municipal Administration of Hospitals Incubation Program","award":["PX2023019"],"award-info":[{"award-number":["PX2023019"]}]},{"name":"Natural Science Foundation of Beijing Municipality","award":["7232047"],"award-info":[{"award-number":["7232047"]}]},{"name":"Natural Science Foundation of Beijing Municipality","award":["7242192"],"award-info":[{"award-number":["7242192"]}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2026,10,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>The clinical phenomenon of metabolic memory, in which diabetic complications may progress despite later glycemic improvement, lacks a complete explanation. Persistent oxidative stress, advanced glycation, mitochondrial dysfunction, and epigenetic remodeling are established contributors, but how these processes intersect with regulated cell death programs is still unresolved.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Main Body:<\/jats:title>\n                    <jats:p>This review proposes and critically appraises the hypothesis that epigenetic dysregulation increases the susceptibility of diabetic tissues to ferroptosis. We employ the term \u201cepigenetic-ferroptosis link\u201d as an operational term denoting a potential mechanistic connection between hyperglycemia-associated chromatin\/RNA-regulatory alterations and shifts in ferroptosis vulnerability. A key methodological tenet of our analysis is the clear demarcation between direct evidence from diabetic models and supportive mechanistic insights drawn from other pathological contexts, ensuring a rigorous assessment of the hypothesis against the available data.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>\n                      Ferroptosis is one execution pathway among several that can contribute to diabetic tissue injury. This framing highlights the critical importance of organ- and cell-type specificity, the experimental rigor required to conclusively demonstrate ferroptosis involvement, the inherent limitations of extracellular-vesicle biomarkers and epigenetic-editing approaches, and the validation steps that remain necessary before any clinical translation can be contemplated.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      45, 534\u2013554.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/15230864261466920","type":"journal-article","created":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T08:36:46Z","timestamp":1783672606000},"page":"534-554","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":1,"title":["From Metabolic Memory to Ferroptotic Susceptibility: A Critical Review of Epigenetic Regulation and Ferroptosis in Diabetic Complications"],"prefix":"10.1177","volume":"45","author":[{"given":"Hongjuan","family":"Fang","sequence":"first","affiliation":[{"name":"Department of Endocrinology, Aviation General Hospital, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4392-0889","authenticated-orcid":false,"given":"Qiang","family":"Wang","sequence":"additional","affiliation":[{"name":"Chinese PLA Center for Disease Control and Prevention, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,7,10]]},"reference":[{"key":"e_1_3_3_2_1","doi-asserted-by":"publisher","DOI":"10.1017\/S0952523820000115"},{"key":"e_1_3_3_3_1","doi-asserted-by":"publisher","DOI":"10.3892\/ijmm.2025.5643"},{"key":"e_1_3_3_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-024-46776-w"},{"key":"e_1_3_3_5_1","doi-asserted-by":"publisher","DOI":"10.3390\/genes16121442"},{"key":"e_1_3_3_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijbiomac.2026.150272"},{"key":"e_1_3_3_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2024.05.007"},{"issue":"2","key":"e_1_3_3_8_1","first-page":"1393","article-title":"Construction and analysis of a lncRNA-miRNA-mRNA network based on competitive endogenous RNA reveals functional lncRNAs in diabetic cardiomyopathy","volume":"20","author":"Chen K","year":"2019","unstructured":"Chen K, , Ma Y, , Wu S, et al. 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