MAFbx/Atrogin-1 is required for atrophic remodeling of the unloaded heart.

ABSTRACT:

Background

Mechanical unloading of the failing human heart induces profound cardiac changes resulting in the reversal of a distorted structure and function. In this process, cardiomyocytes break down unneeded proteins and replace those with new ones. The specificity of protein degradation via the ubiquitin proteasome system is regulated by ubiquitin ligases. Over-expressing the ubiquitin ligase MAFbx/Atrogin-1 in the heart inhibits the development of cardiac hypertrophy, but the role of MAFbx/Atrogin-1 in the unloaded heart is not known.

Methods and results

Mechanical unloading, by heterotopic transplantation, decreased heart weight and cardiomyocyte cross-sectional area in wild type mouse hearts. Unexpectedly, MAFbx/Atrogin-1(-/-) hearts hypertrophied after transplantation

SUBMITTER: Baskin KK 

PROVIDER: S-EPMC4037330 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature