The size of a cardiomyocyte is determined by relative rates of protein synthesis and degradation. Signaling pathways regulating myocardial protein synthesis have been extensively investigated, not the least because in patients hypertrophy increases cardiovascular morbidity and mortality. Until now strategies to reverse hypertrophy have relied on the inhibition of prohypertrophic signaling pathways. Here we review signaling pathways of atrophy in the heart and we present evidence in support of the idea that activating proatrophic signaling pathways in the presence of prohypertrophic signaling may be an attractive strategy to reverse hypertrophy.
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