CaMKII exacerbates heart failure progression by activating class I HDACs.

ABSTRACT:

Background

Persistent cardiac Ca²⁺/calmodulin dependent Kinase II (CaMKII) activation plays an essential role in heart failure development. However, the molecular mechanisms underlying CaMKII induced heart failure progression remains incompletely understood. Histone deacetylases (HDACs) are critical for transcriptional responses to stress, and contribute to expression of pathological genes causing adverse ventricular remodeling. Class I HDACs, including HDAC1, HDAC2 and HDAC3, promote pathological cardiac hypertrophy, whereas class IIa HDACs suppress cardiac hypertrophy. While it is known that CaMKII deactivates class IIa HDACs to enhance cardiac hypertrophy, the role of CaMKII in regulating class I HDACs during heart failure progression is unclear.

Methods and result

SUBMITTER: Zhang M 

PROVIDER: S-EPMC7736490 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature