Animal modeling of cardiac steatosis presented with myocardial infarction and heart failure reduced VDR activity causes increased expression of diacylglycerol acyltransferase 1, atrial natriuretic, and B-type natriuretic peptides, collagen 1a, and 3a, osteopontin, matrix metalloproteinase (MMP) and tissue growth factor-beta (TGF-β) thereby, increasing lipotoxicity, fibrosis, and hypertrophy of cardiac myocytes. Here, VDR is linked to heart failure.