Selective knockout of the vitamin d receptor in the heart results in cardiac hypertrophy: is the heart a drugable target for vitamin D receptor agonists?

The report by Dr Chen and colleagues, published in this issue of Circulation, “Cardiomyocyte-Specific Deletion of the Vitamin D Receptor Gene Results In Cardiac Hypertrophy,” is important and timely.1 This study extends and supports other studies that have demonstrated that vitamin D and the vitamin D receptor (VDR) signaling system possess antihypertrophic activity in the heart. The study also furthers our knowledge of this action by demonstrating an involvement of the prohypertrophic calcineurin/nuclear factor of activated T-cells/modulatory calcineurin-interacting protein-1 pathway. Thereby, they identify a potential mechanism to account for the reported beneficial effects of vitamin D on the cardiovascular system. To respond to the question posed in the title of this editorial, “Is the heart a drugable target for vitamin D receptor agonists?” Chen et al’s report makes an affirmative response more plausible.