Abstract
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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