PGC-1β deficiency accelerates the transition to heart failure in pressure overload hypertrophy.

ABSTRACT:

Rationale

Pressure overload cardiac hypertrophy, a risk factor for heart failure, is associated with reduced mitochondrial fatty acid oxidation (FAO) and oxidative phosphorylation (OXPHOS) proteins that correlate in rodents with reduced PGC-1α expression.

Objective

To determine the role of PGC-1β in maintaining mitochondrial energy metabolism and contractile function in pressure overload hypertrophy.

Methods and results

PGC-1β deficient (KO) mice and wildtype (WT) controls were subjected to transverse aortic constriction (TAC). Although LV function was modestly reduced in young KO hearts, there was no further decline with age so that LV function was similar between KO and WT when TAC was performed. WT-TAC mice developed relatively compensated LVH, despite reduced mito

SUBMITTER: Riehle C 

PROVIDER: S-EPMC3175248 | biostudies-literature | 2011 Sep

REPOSITORIES: biostudies-literature