{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T23:48:11Z","timestamp":1791589691012,"version":"4.3.4"},"reference-count":345,"publisher":"SAGE Publications","issue":"13-15","license":[{"start":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T00:00:00Z","timestamp":1770940800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2026,5,1]]},"abstract":"<jats:sec>\n                    <jats:title>Significance:<\/jats:title>\n                    <jats:p>Ferroptosis, an iron- and lipid peroxidation-dependent mode of programmed cell death, is presently realized as a converging mediator that bridges redox imbalance and metabolic dysfunction. Differing from apoptosis and necroptosis, ferroptosis involves iron homeostasis, glutathione depletion, and redox lipid damage. Thus, it becomes the intersection of metabolic reprogramming and redox signaling. Ferroptosis is a double-edged metabolic vulnerability and adaptive resistance pathway in malignancy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Recent Advances:<\/jats:title>\n                    <jats:p>\n                      Oncogenic signaling cascades such as PI3K\/Akt\/mTOR and AMPK restructure glucose and lipid metabolism to regulate ferroptotic sensitivity, whereas cancer cells destabilize antioxidant defense pathways such as X\n                      <jats:sc>c<\/jats:sc>\n                      <jats:sup>\u2212<\/jats:sup>\n                      -GSH-GPX4 and FSP1-CoQ10-NAD(P)H pathways to evade ferroptotic cell death. Pharmacological inducers erastin, RSL3, and sorafenib reverse oxidative imbalance, enhance antitumor effect, and immune modulation in the tumor microenvironment. In diabetic mellitus complications, ferroptosis is responsible for \u03b2-cell deterioration, insulin resistance, and vascular injury. Hyperglycemia-induced oxidative stress and dysregulated GPX4 facilitate lipid peroxidation and ferroptotic cell death in pancreatic \u03b2-cells, while iron overload and mitochondrial dysfunctions facilitate ferroptotic injury in diabetic cardiomyopathy, nephropathy, retinopathy, and foot ulcer. These observations position ferroptosis as a crucial metabolically reorganized hub of organ damage.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Critical Issues:<\/jats:title>\n                    <jats:p>Despite rapid advancements, foundational challenges persist, including the identification of ferroptosis-specific biomarkers, tissue-specific thresholds, and mechanisms for neutralizing off-target toxicity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Future Directions:<\/jats:title>\n                    <jats:p>\n                      Recently developed technologies such as CRISPR-based functional genomics, metabolomics, and AI-powered modeling represent new-age tools in defining ferroptosis networks and precision therapeutics design. Integration of the regulation of normal physiological ferroptosis into cancer and diabetes therapy has the potential to redefine redox-targeted therapy and metabolic medicine.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      44, 676\u2013711.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/15230864261421487","type":"journal-article","created":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T08:20:47Z","timestamp":1770970847000},"page":"676-711","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":3,"title":["Metabolic Reprogramming and Ferroptosis: Unlocking New Therapeutic Frontiers in Cancer and Diabetes"],"prefix":"10.1177","volume":"44","author":[{"given":"Yan","family":"Huo","sequence":"first","affiliation":[{"name":"Suzhou Chien-Shiung Institute of Technology, Suzhou, China."},{"name":"Jiangsu Provincial Novel Anti-Tumor Targeted Drug Conjugate Engineering Research Center, Suzhou, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaoxiong","family":"Xia","sequence":"additional","affiliation":[{"name":"Departments of 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China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhun","family":"Gu","sequence":"additional","affiliation":[{"name":"Suzhou Chien-Shiung Institute of Technology, Suzhou, China."},{"name":"Jiangsu Provincial Novel Anti-Tumor Targeted Drug Conjugate Engineering Research Center, Suzhou, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nannan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, the Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer Hospital, Zhengzhou, Henan, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4234-0981","authenticated-orcid":false,"given":"Yanping","family":"Gao","sequence":"additional","affiliation":[{"name":"Departments of Radiotherapy, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Peking University Cancer Hospital Yunnan, Kunming, Yunnan, 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