{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T19:51:04Z","timestamp":1780084264771,"version":"3.54.0"},"reference-count":52,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T00:00:00Z","timestamp":1772928000000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T00:00:00Z","timestamp":1772323200000},"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":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Acute kidney injury (AKI) is a common and severe complication of sepsis and represents an independent risk factor for mortality in septic patients. Despite its clinical significance, the mechanisms of sepsis\u2010induced AKI (Sepsis\u2010AKI) remain incompletely understood. This study investigates the role of methyltransferase like 14 (METTL14)\u2010mediated m6A modification in regulating brain and muscle ARNT\u2010like protein\u20101 (BMAL1) stability and its effect on tubular epithelial cell injury and ferroptosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Human renal proximal tubular epithelial (HK\u20102) cells were treated with lipopolysaccharide (LPS) to establish an in\u00a0vitro model of Sepsis\u2010AKI. Cell proliferation and viability were assessed using EdU and CCK\u20108 assays; apoptosis was evaluated by TUNEL staining, and inflammatory cytokines Interleukin\u20106 (IL\u20106) and IL\u20101\u03b2 were measured by ELISA. Ferroptosis indices were detected using corresponding kits. RT\u2010qPCR and Western blotting were used to detect mRNA and protein expression. MeRIP and RIP assays were used to evaluate BMAL1 m6A modification and RNA\u2010protein interaction. The stability of BMAL1 mRNA was determined using an Actinomycin D chase assay. A Sepsis\u2010AKI model was established to examine the effect of METTL14 silencing on renal injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>BMAL1 overexpression significantly alleviated LPS\u2010induced apoptosis, inflammatory responses, and ferroptosis in HK\u20102 cells. Furthermore, METTL14 silencing reduced BMAL1 m6A modification, stabilized BMAL1 mRNA, and consequently improved HK\u20102 cell injury. In addition, YTHN6\u2010methyladenosine RNA binding protein 1 (YTHDF1) was identified as the critical m6A reader mediating BMAL1 mRNA degradation. Consistently, in\u00a0vivo experiments demonstrated that METTL14 knockdown mitigated Sepsis\u2010AKI and ferroptosis in mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>METTL14 enhanced BMAL1 m6A modification and promoted YTHDF1\u2010mediated BMAL1 degradation, thereby facilitating ferroptosis and aggravating Sepsis\u2010AKI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/1440-1681.70107","type":"journal-article","created":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T06:15:31Z","timestamp":1773036931000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["<scp>METTL14<\/scp>\n                    Aggravates Sepsis\u2010Induced Acute Kidney Injury by Promoting Ferroptosis Through\n                    <scp>m6A<\/scp>\n                    Modification of\n                    <scp>BMAL1<\/scp>"],"prefix":"10.1111","volume":"53","author":[{"given":"Yishu","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Comprehensive Internal Medicine Beijing Xiaotangshan Hospital  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Comprehensive Internal Medicine Beijing Xiaotangshan Hospital  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Na","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Comprehensive Internal Medicine Beijing Xiaotangshan Hospital  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinyue","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Comprehensive Internal Medicine Beijing Xiaotangshan Hospital  Beijing 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