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Cardiomyocyte-specific YTHDF1 deficiency leads to maladaptive cardiac remodeling in response to swimming exercise and additionally exacerbates pathological cardiac remodeling under pressure overload stimulation in vivo. In vitro, YTHDF1 functions as a switch to regulate the type of cardiomyocyte hypertrophy in an RNA m\n                    <jats:sup>6<\/jats:sup>\n                    A-dependent manner. Mechanistically, the YTHDF1\u2013KLF11\u2013HIF1\u03b1 axis contributes to metabolic adaptation during cardiomyocyte hypertrophy. Cardiac-specific overexpression of YTHDF1 alleviates pathological cardiac remodeling. Together, our findings reveal a previously unrecognized YTHDF1\u2013KLF11\u2013HIF1\u03b1 regulatory pathway linking m\n                    <jats:sup>6<\/jats:sup>\n                    A RNA recognition to cardiomyocyte remodeling. These findings provide valuable insight into how m\n                    <jats:sup>6<\/jats:sup>\n                    A-dependent signaling coordinates stress-responsive cardiac adaptation and establish YTHDF1 as an important regulator of cardiomyocyte remodeling.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2603028123","type":"journal-article","created":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T17:58:11Z","timestamp":1788285491000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":0,"title":["YTHDF1-mediated m\n                    <sup>6<\/sup>\n                    A RNA regulation controls cardiomyocyte remodeling through 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