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Multiple genetic risk factors have been reported to be associated with the development of FSGS. However, whether epigenetic factors, especially N6\u2010methyladenosine (m6A) modifications, are involved in the pathogenesis of FSGS remains unclear. By generating a mouse line with a specific deletion of N6\u2010adenosine\u2010methyltransferase\u2010like 3 (\n                    <jats:italic>Mettl3<\/jats:italic>\n                    ) in podocytes (\n                    <jats:italic>Mettl3<\/jats:italic>\n                    <jats:sup>podko<\/jats:sup>\n                    mice), podocytes are isolated and performed RNA\u2010seq. It is shown that RNA m6A methylation levels are reduced in the renal glomeruli of both animal models and patients with FSGS. A significant decrease in RNA m6A levels in podocytes and the development of an FSGS phenotype are observed in the\n                    <jats:italic>Mettl3<\/jats:italic>\n                    <jats:sup>podko<\/jats:sup>\n                    mice. Furthermore, RNA\u2010seq and m6A\u2010immunoprecipitated RNA sequencing revealed that silencing\n                    <jats:italic>Mettl3<\/jats:italic>\n                    expression in podocytes led to a gene expression profile associated with slit diaphragm dysfunction. RNA immunoprecipitation assay and hybridization chain reaction (HCR) analysis further identified the slit diaphragm marker TJP1 as a potential target of Mettl3. Moreover, loss\u2010 and gain\u2010of\u2010function analyses showed that Mettl3 enhances podocyte RNA m6A modification, probably through the TJP1\u2013CDC42 pathway. Finally, treatment of\n                    <jats:italic>Mettl3<\/jats:italic>\n                    <jats:sup>podko<\/jats:sup>\n                    and adriamycin (ADR)\u2010induced FSGS mice with m6A\u2010mimic compounds markedly ameliorated the progression of FSGS. The findings demonstrate that\n                    <jats:italic>Mettl3<\/jats:italic>\n                    \u2010mediated RNA m6A modification is essential for maintaining podocyte architecture and function and represents a potential therapeutic target for FSGS.\n                  <\/jats:p>","DOI":"10.1002\/advs.202501242","type":"journal-article","created":{"date-parts":[[2025,12,19]],"date-time":"2025-12-19T17:52:16Z","timestamp":1766166736000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["<i>Mettl3<\/i>\n                    \u2010Mediated m6A Modification Represents a Novel Therapeutic Target for FSGS"],"prefix":"10.1002","volume":"13","author":[{"given":"Fubin","family":"Zhu","sequence":"first","affiliation":[{"name":"Nephrosis Precision Medicine Innovation Center School of Basic Medicine, Beihua University Jilin 132011 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