{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T15:28:31Z","timestamp":1791646111858,"version":"4.3.4"},"reference-count":77,"publisher":"SAGE Publications","issue":"7-9","license":[{"start":{"date-parts":[[2023,6,5]],"date-time":"2023-06-05T00:00:00Z","timestamp":1685923200000},"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":[[2024,3]]},"abstract":"<jats:sec>\n                    <jats:title>Aims:<\/jats:title>\n                    <jats:p>Diabetic kidney disease (DKD) is the leading cause of end-stage kidney disease. Sodium\u2013glucose cotransporter 2 inhibitors (SGLT2i) showed excellent renoprotective effects; however, the underlying mechanism remains not fully understood. Previous studies have revealed the importance of ferroptosis, which is closely related to oxidative stress, in the progression of DKD. In the current study, we hypothesized that SGLT2i could relieve ferroptosis and thereby alleviate renal injury in DKD due to their antioxidative stress effects.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Typical changes of ferroptosis including massive lipid peroxidation, compromised antioxidant capability, and iron overload were found in\n                      <jats:italic toggle=\"yes\">db\/db<\/jats:italic>\n                      mice and high glucose\/high fat (HG\/HF)-treated HK-2 cells. Furthermore, increased expression of hypoxia inducible factor 1\u03b1 (HIF1\u03b1) and heme oxygenase 1 (HO1) was observed in\n                      <jats:italic toggle=\"yes\">db\/db<\/jats:italic>\n                      mice and HG\/HF-treated HK-2 cells as well. Dapagliflozin treatment significantly ameliorated the ferroptosis-related changes\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      attenuating overactivation of the HIF1\u03b1\/HO1 axis\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      . Besides, downregulation of the HIF1\u03b1\/HO1 axis alleviated ferroptosis, while overexpression of HIF1\u03b1 and HO1 aggravated ferroptosis induced by HG\/HF in HK-2 cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Innovation and Conclusion:<\/jats:title>\n                    <jats:p>\n                      This study revealed that SGLT2i played a renoprotective role in DKD, at least in part, through alleviating HIF1\u03b1\/HO1-mediated ferroptosis.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      40, 492\u2013509.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/ars.2022.0169","type":"journal-article","created":{"date-parts":[[2023,6,5]],"date-time":"2023-06-05T13:02:20Z","timestamp":1685970140000},"page":"492-509","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":57,"title":["Dapagliflozin Alleviates Diabetic Kidney Disease\n                    <i>via<\/i>\n                    Hypoxia Inducible Factor 1\u03b1\/Heme Oxygenase 1-Mediated Ferroptosis"],"prefix":"10.1177","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8511-3017","authenticated-orcid":false,"given":"Yi-hui","family":"Wang","sequence":"first","affiliation":[{"name":"Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China."},{"name":"Peking-Tsinghua Center for Life Sciences, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong-yuan","family":"Chang","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China."},{"name":"Research Units of Diagnosis and Treatment of Immune-Mediated Kidney Diseases, Chinese Academy of Medical Sciences, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming-hui","family":"Zhao","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China."},{"name":"Peking-Tsinghua Center for Life Sciences, Beijing, China."},{"name":"Research Units of Diagnosis and Treatment of Immune-Mediated Kidney Diseases, Chinese Academy of Medical Sciences, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Chen","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China."},{"name":"Research Units of Diagnosis and Treatment of Immune-Mediated Kidney Diseases, Chinese Academy of Medical 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