Key result
METTL3 inhibition improves post-MI cardiac function and reduces fibrosis by decreasing β-catenin mRNA methylation.
Why the study?
Does METTL3 inhibition reduce myofibroblast activation and adverse remodeling following myocardial infarction in preclinical models?
Does METTL3 inhibition reduce myofibroblast activation and adverse remodeling following myocardial infarction in preclinical models?
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Inhibition of METTL3-mediated mRNA methylation reduces MI-induced cardiac fibrosis and improves cardiac function, highlighting a potential novel therapeutic pathway for heart failure.
Dutta et al. (2025) studied Myocardial infarction and cardiac fibrosis. METTL3 inhibition (STM 2457 or genetic knockout) vs. Sham or control was evaluated on Cardiac function (ejection fraction and fractional shortening) and fibrosis. METTL3 inhibition via STM 2457 or genetic knockout improved cardiac function and reduced fibrosis post-myocardial infarction by decreasing β-catenin mRNA methylation.
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