FHL2 switches MITF from activator to repressor of Erbin expression during cardiac hypertrophy.

ABSTRACT:

Background

Congestive heart failure (CHF) is a significant health care burden in developed countries. However, the molecular events leading from cardiac hypertrophy to CHF are unclear and preventive therapeutic approaches are limited. We have previously described that microphthalmia-associated transcription factor (MITF) is a key regulator of cardiac hypertrophy, but its cardiac targets are still uncharacterized.

Methods and results

Gene array analysis of hearts from MITF-mutated mice indicated that ErbB2 interacting protein (Erbin) is a candidate target gene for MITF. We have recently demonstrated that Erbin is decreased in human heart failure and plays a role as a negative modulator of pathological cardiac hypertrophy. Here we show that Erbin expression is regulated by MIT

SUBMITTER: Rachmin I 

PROVIDER: S-EPMC4478144 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature