Epigenetic regulation of E2F-1-dependent Bnip3 transcription and cell death by nuclear factor-κB and histone deacetylase-1.

A delicate balance exists between cell growth and cell death. In the context of the adult myocardium, inappropriate or inordinate cell loss through an apoptotic process may profoundly influence cardiac structure, function, or both given the limited and meager ability of the heart for repair after injury. Earlier work by the authors' laboratory identified a close relation between cell cycle factor E2F-1 and hypoxia-inducible factor Bnip3 as the key regulator of apoptosis and autophagy in ventricular myocytes. Epigenetic changes by histone-modifying proteins, namely, histone deacetylases (HDACs) influence cell survival by altering the activity of histone core proteins, transcription factors, or both. This report highlights the intricate nature between the cellular factors E2F-1 and nuclear factor-κB (NF-κB) and the epigenetic regulation of Bnip3 gene transcription by HDAC1 for cell survival of ventricular myocytes.