Titrating autophagy in cardiac plasticity.

The heart is a highly plastic organ. In a recent study, we found that autophagy is a required element in load-induced cardiomyocyte growth; when autophagy is suppressed, the heart does not grow. Conversely, afterload stress triggers a transient increase in cardiomyocyte autophagic activity which settles to a new--higher--baseline once the heart has re-achieved steady-state size. Our work went on to decipher the role of histone deacetylases in this biology.