CIP, a cardiac Isl1-interacting protein, represses cardiomyocyte hypertrophy.

ABSTRACT:

Rationale

Mammalian heart has minimal regenerative capacity. In response to mechanical or pathological stress, the heart undergoes cardiac remodeling. Pressure and volume overload in the heart cause increased size (hypertrophic growth) of cardiomyocytes. Whereas the regulatory pathways that activate cardiac hypertrophy have been well-established, the molecular events that inhibit or repress cardiac hypertrophy are less known.

Objective

To identify and investigate novel regulators that modulate cardiac hypertrophy.

Methods and results

Here, we report the identification, characterization, and functional examination of a novel cardiac Isl1-interacting protein (CIP). CIP was identified from a bioinformatic search for novel cardiac-expressed genes in mouse embryonic hearts

SUBMITTER: Huang ZP 

PROVIDER: S-EPMC3307880 | biostudies-literature | 2012 Mar

REPOSITORIES: biostudies-literature