PPARGC1A and cardiomyopathy: Transgenic mice with myocardial inactivation/deletion/deficiency of total PGC-1α develop a dilatative cardiomyopathy phenotype with increased end systolic volume and reduced contractile function as well as metabolic alterations associated with heart failure [24], while overexpression of PGC-1α-a appears to enhance contractility without negative feedback on cardiac metabolism [25].