The objectives of the present study were to test the hypotheses that: a) HF increases expression of TSPO, with a concomitant decrease in inward mitochondrial Ca2+ entry and systolic function; and thus b) genetic modulation of the TSPO could normalize mitochondrial Ca2+ uptake and prevent the abnormalities in cardiac structure and function evident in HF, specifically by normalizing cellular energetics and redox balance inside cardiomyocytes. This evidence concerns the gene TSPO and hydrops fetalis.