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Accumulating studies demonstrate that injury to renal tubular epithelial cells (RTECs) is central to the onset and progression of AKI, as well as a key driver of the transition from AKI to chronic kidney disease (CKD). Glycine amidinotransferase (GATM) is the rate-limiting enzyme in creatine synthesis, but its role in AKI remains unknown. This study therefore investigates the regulatory role and molecular mechanism of GATM in AKI.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>GATM expression was assessed in single-cell datasets, AKI mouse models, and patient biopsies. GATM-knockout and adeno-associated virus-mediated overexpression mice were used to evaluate its functional role in vivo, alongside in vitro studies in HK-2 cells and primary RTECs. Mechanistic investigations integrated experiments on transcriptomic sequencing, lipophagy, and regulation of creatine synthesis. Upstream regulation was explored via m6A dot blot and siRNA-mediated knockdown, with a focus on the METTL14\/YTHDF2\u2013GATM axis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>GATM was significantly downregulated in RTECs across AKI models and patients, with expression correlating positively with renal function. GATM knockout exacerbated AKI, whereas overexpression ameliorated injury and attenuated progression to CKD. Mechanistically, GATM overexpression promoted lipophagy via enhanced creatine synthesis, and these effects were reversed by autophagy inhibitor 3-methyladenine or creatine synthesis blockade. Upstream, METTL14\/YTHDF2-mediated m6A methylation contributed to GATM downregulation, and their knockdown restored GATM expression and alleviated renal injury in AKI.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings suggest that GATM may play a protective role in AKI, potentially through promoting lipophagy via creatine synthesis. Its downregulation via METTL14\/YTHDF2-mediated m6A methylation may contribute to tubular injury. The METTL14\/YTHDF2\u2013GATM axis may represent a promising candidate for further therapeutic exploration in AKI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ndt\/gfag226","type":"journal-article","created":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T11:37:10Z","timestamp":1791027430000},"source":"Crossref","is-referenced-by-count":0,"title":["GATM-mediated creatine synthesis alleviates acute kidney injury by promoting lipophagy in renal tubular epithelial cells"],"prefix":"10.1093","author":[{"given":"Xu","family":"Guan","sequence":"first","affiliation":[{"name":"Department of Nephrology, Chongqing Key Laboratory of Prevention and Treatment of Kidney Disease, Chongqing Clinical Research Center of Kidney and Urology Diseases, Xinqiao Hospital, Army Medical University (Third Military Medical University) , Chongqing ,","place":["China"]},{"name":"Department of Nephrology, Chongqing Traditional Chinese Medicine Hospital , Chongqing 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