{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T12:17:21Z","timestamp":1787314641807,"version":"build-2736575974"},"reference-count":58,"publisher":"Wiley","issue":"43","license":[{"start":{"date-parts":[[2024,9,20]],"date-time":"2024-09-20T00:00:00Z","timestamp":1726790400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82204493"],"award-info":[{"award-number":["82204493"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003995","name":"Natural Science Foundation of Anhui Province","doi-asserted-by":"publisher","award":["2208085QH237"],"award-info":[{"award-number":["2208085QH237"]}],"id":[{"id":"10.13039\/501100003995","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2024,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Several studies have observed renal cell ferroptosis during cisplatin\u2010induced acute kidney injury (AKI). However, the mechanism is not completely clear. In this study, oxidized arachidonic acid (AA) metabolites are increased in cisplatin\u2010treated HK\u20102 cells. Targeted metabolomics showed that the end product of pyrimidine biosynthesis is decreased and the initiating substrate of pyrimidine biosynthesis is increased in cisplatin\u2010treated mouse kidneys. Mitochondrial DHODH, a key enzyme for pyrimidine synthesis, and its downstream product CoQH\n                    <jats:sub>2<\/jats:sub>\n                    , are downregulated. DHODH overexpression attenuated but DHODH silence exacerbated cisplatin\u2010induced CoQH\n                    <jats:sub>2<\/jats:sub>\n                    depletion and lipid peroxidation. Mechanistically, renal DHODH acetylation is elevated in cisplatin\u2010exposed mice. Mitochondrial SIRT3 is reduced in cisplatin\u2010treated mouse kidneys and HK\u20102 cells. Both in vitro SIRT3 overexpression and in vivo NMN supplementation attenuated cisplatin\u2010induced mitochondrial DHODH acetylation and renal cell ferroptosis. By contrast,\n                    <jats:italic>Sirt3<\/jats:italic>\n                    knockout aggravated cisplatin\u2010induced mitochondrial DHODH acetylation and renal cell ferroptosis, which can not be attenuated by NMN. Additional experiments showed that cisplatin caused mitochondrial dysfunction and SIRT3 SUMOylation. Pretreatment with mitochondria\u2010target antioxidant MitoQ alleviated cisplatin\u2010caused mitochondrial dysfunction, SIRT3 SUMOylation, and DHODH acetylation. MitoQ pretreatment protected against cisplatin\u2010caused AKI and renal cell ferroptosis. Taken together, these results suggest that mitochondrial dysfunction\u2010evoked DHODH acetylation partially contributes to renal cell ferroptosis during cisplatin\u2010induced AKI.\n                  <\/jats:p>","DOI":"10.1002\/advs.202404753","type":"journal-article","created":{"date-parts":[[2024,11,20]],"date-time":"2024-11-20T14:20:06Z","timestamp":1732112406000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["Mitochondrial Dysfunction\u2010Evoked DHODH Acetylation is Involved in Renal Cell Ferroptosis during Cisplatin\u2010Induced Acute Kidney Injury"],"prefix":"10.1002","volume":"11","author":[{"given":"Nan\u2010Nan","family":"Liang","sequence":"first","affiliation":[{"name":"Department of Toxicology Anhui Medical University  Hefei China 230032"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue\u2010Yue","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Toxicology Anhui Medical University  Hefei China 230032"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao\u2010Yi","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Toxicology Anhui Medical University  Hefei China 230032"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ya\u2010Hui","family":"Ren","sequence":"additional","affiliation":[{"name":"Department of Urology the Second Affiliated Hospital of Anhui Medical University  Hefei China 230601"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi\u2010Zhang","family":"He","sequence":"additional","affiliation":[{"name":"Department of Urology the Second Affiliated Hospital of Anhui Medical University  Hefei China 230601"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi\u2010Bing","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Blood Transfusion Second Affiliated Hospital of Anhui Medical University  Hefei Anhui 230601 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5126-4335","authenticated-orcid":false,"given":"De\u2010Xiang","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Toxicology Anhui Medical University  Hefei China 230032"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0520-9511","authenticated-orcid":false,"given":"Shen","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Urology the Second Affiliated Hospital of Anhui Medical University  Hefei China 230601"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2024,9,20]]},"reference":[{"key":"e_1_2_9_1_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41572-021-00284-z"},{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.328"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.294.7.813"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbagen.2013.12.007"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.5.F726"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0959-8049(98)00224-X"},{"key":"e_1_2_9_7_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41419-020-2256-z"},{"key":"e_1_2_9_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jsbmb.2020.105789"},{"key":"e_1_2_9_9_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms20205238"},{"key":"e_1_2_9_10_1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014080741"},{"key":"e_1_2_9_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2012.03.042"},{"key":"e_1_2_9_12_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI129903"},{"key":"e_1_2_9_13_1","doi-asserted-by":"crossref","DOI":"10.1016\/j.fct.2021.112672","volume":"158","author":"Yu M.","year":"2021","journal-title":"Food and chemical Toxicol.: An Int. 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