Key result
FOXP1 restricts MEF2A activation via the p38MAPK pathway, potentially preventing gene reactivation in cardiomyocyte hypertrophy.
FOXP1 restricts MEF2A function, preventing premature differentiation in myogenic progenitors and potentially preventing re-activation of embryonic gene expression during cardiomyocyte hypertrophy.
Does not support clinical translation; leaves open mechanistic relevance of FOXP1-MEF2A in human hypertrophy.
activation properties and myogenin expression. The FoxP1:MEF2A interaction is also preserved in cardiomyocytes and FoxP1 depletion enhanced cardiomyocyte hypertrophy. FOXP1 prevented MEF2A phosphorylation and activation by the p38MAPK pathway. Overall, these data implicate FOXP1 in restricting MEF2A function in order to avoid premature differentiation in myogenic progenitors and also to possibly prevent re-activation of embryonic gene expression in cardiomyocyte hypertrophy.
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Steiman et al. (2024) studied Cardiomyocyte hypertrophy. FoxP1 depletion was evaluated on MEF2A phosphorylation and activation. FOXP1 restricts MEF2A function by preventing its phosphorylation and activation via the p38MAPK pathway, potentially preventing embryonic gene expression re-activation in cardiomyocyte hypertrophy.
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