{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T07:17:42Z","timestamp":1784791062091,"version":"3.55.0"},"reference-count":51,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T00:00:00Z","timestamp":1777420800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T00:00:00Z","timestamp":1777420800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82360218"],"award-info":[{"award-number":["82360218"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82160212"],"award-info":[{"award-number":["82160212"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical &amp; Translational Med"],"published-print":{"date-parts":[[2026,5]]},"abstract":"Abstract<\/jats:title>\n \n Background<\/jats:title>\n RNA\u2010binding proteins (RBPs) and ferroptosis have been demonstrated to play important roles in the progression of chronic rhinosinusitis (CRS). However, the regulatory mechanisms underlying the interaction between RBPs and ferroptosis in CRS, particularly regarding mitochondrial metabolism, remain elusive.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n Hub genes correlated with RBP\u2010related genes, ferroptosis\u2010related genes and mitochondrial\u2010related genes were identified by integrated bioinformatics analysis. CRS in vivo models were constructed, clinical samples were collected, and mechanistic analyses were performed for validation.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n ZFP36L1<\/jats:italic>\n was identified as the hub gene associated with CRS development. In vivo experiments demonstrated that\n ZFP36L1<\/jats:italic>\n directly binds to the 3\u2032\u2010untranslated region of\n CAMK2A<\/jats:italic>\n mRNA and promotes its degradation through AU\u2010rich element recognition.\n ZFP36L1<\/jats:italic>\n knockout in CRS mouse models restored\n CAMK2A<\/jats:italic>\n expression and significantly attenuated ferroptosis markers, reactive oxygen species accumulation and mitochondrial dysfunction. Rescue experiments revealed that\n CAMK2A<\/jats:italic>\n knockdown reversed the protective effects of\n ZFP36L1<\/jats:italic>\n depletion on ferroptosis and mitochondrial quality control. Clinical samples confirmed that ZFP36L1 expression was inversely correlated with CAMK2A levels, and both were associated with disease severity.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n \n This study identifies\n ZFP36L1\u2013CAMK2A<\/jats:italic>\n as a contributory regulatory mechanism in CRS pathogenesis.\n ZFP36L1<\/jats:italic>\n promotes ferroptosis by destabilizing\n CAMK2A<\/jats:italic>\n mRNA, leading to mitochondrial dysfunction and subsequent epithelial cell death. These findings provide new mechanistic insights into CRS progression and identify potential therapeutic targets.\n <\/jats:p>\n <\/jats:sec>\n \n Highlights<\/jats:title>\n \n \n \n ZFP36L1 is identified as a key driver gene in chronic rhinosinusitis (CRS) progression via integrated bioinformatics analysis.<\/jats:p>\n <\/jats:list-item>\n \n ZFP36L1 promotes ferroptosis by binding to and destabilizing CAMK2A mRNA through AU\u2010rich elements in its 3'\u2010UTR.<\/jats:p>\n <\/jats:list-item>\n \n Genetic knockout of ZFP36L1 attenuates ferroptosis and restores mitochondrial quality control in CRS models.<\/jats:p>\n <\/jats:list-item>\n \n Clinical validation confirms the ZFP36L1\u2010CAMK2A axis correlates with disease severity and represents a potential therapeutic target.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n 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