Addition, in a transgenic mouse model, myocardial-specific PGC1α overexpression resulted in excessive mitochondrial proliferation and disruption of sarcoplasmic reticulum structure in cardiomyocytes, leading to cardiac enlargement with reduced myocardial contractile function (128), which indicate the overexpression of PGC1α does not improve mitochondrial function (129).This may be explained by the fact that the outcome of PGC1α overexpression and its effects on HF are tightly related to the activity and the interaction of mitochondrial biogenesis with other intracellular events. This evidence concerns the gene PPARGC1A and hydrops fetalis.