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In severe or recurrent cases, AKI can progress to chronic kidney disease (CKD), marked by renal inflammation and fibrosis. Despite the severity of these outcomes, early-stage diagnostic tools and pharmacological interventions for AKI-to-CKD progression remain limited. In this study, we examined circular RNA (circRNA) expression profiles in mouse renal cortex tissues 14 days after ischemia\/reperfusion (I\/R) injury using circRNA-Seq. The renal biopsy samples of patients after AKI exhibited reduced\n                    <jats:italic>CircNSD1<\/jats:italic>\n                    expression, which was inversely associated with inflammation and fibrosis. Overexpression of\n                    <jats:italic>CircNSD1<\/jats:italic>\n                    attenuated ferroptosis in vivo and in vitro, while slowing AKI-to-CKD progression. Mechanistically,\n                    <jats:italic>CircNSD1<\/jats:italic>\n                    downregulated\n                    <jats:italic>ACSL4<\/jats:italic>\n                    and\n                    <jats:italic>SLC39A14<\/jats:italic>\n                    expression through histone H3 lysine 36 (H3K36) methylation, a critical pathway regulating ferroptosis after AKI or hypoxia\/reoxygenation (H\/R) injury. Furthermore, we identified that\n                    <jats:italic>CircNSD1<\/jats:italic>\n                    encoded a NSD1-916aa peptide, which may functionally contribute to its observed effect. Collectively, these findings demonstrated that Circ\n                    <jats:italic>NSD1<\/jats:italic>\n                    may serve as a diagnostic and therapeutic target for early detection of AKI-to-CKD transition.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.189130","type":"journal-article","created":{"date-parts":[[2025,7,15]],"date-time":"2025-07-15T17:11:57Z","timestamp":1752599517000},"source":"Crossref","is-referenced-by-count":3,"title":["NSD1-916aa encoded by CircNSD1 contributes to AKI-to-CKD transition through inducing ferroptosis in tubular epithelial cells"],"prefix":"10.1172","volume":"10","author":[{"given":"Li","family":"Gao","sequence":"first","affiliation":[{"name":"Inflammation and Immune-Mediated Diseases Laboratory of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, and"},{"name":"Department of Nephropathy, The First Affiliated Hospital of Anhui Medical University, Hefei, China."},{"name":"Center for Scientific Research 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