Titrating autophagy in cardiac plasticity

摘要

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.