Titrating autophagy in cardiac plasticity

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1078-1079
Number of pages2
Issue number9
StatePublished - Sep 2011


  • Heart
  • Heart failure
  • Histone deacetylase
  • Hypertrophy
  • Remodeling

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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