Abstract Thu097: METTL3 inhibition reduces myofibroblast activation and adverse remodeling following MI.

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Discussion

Research shows METTL3 plays a crucial role in fibrosis after ischemia, indicating potential therapies for cardiac repair.

Inhibition of METTL3 results in reduced cardiac fibrosis following myocardial infarction, improving heart function.
Analysis revealed increased β-catenin mRNA methylation, contributing to enhanced fibrosis after MI events.
Using myoFB METTL3 knockout mice and pharmacological inhibition, the effect on cardiac function and fibrosis was assessed.
These findings highlight METTL3's regulatory role in mRNA stability and its potential as a therapeutic target for heart failure.

Dutta et al. (2025) studied this question.

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