Similarly, the improvement in cardiac function in response toparicalcitol treatment of mice following induction of myocardial infarction, hasalso been shown to be related to a reduction in apoptosis and inflammation [35].Furthermore, VDR protein and mRNA levels were restored by paricalcitol treatment.Taken together, it is apparent that the cardioprotective effects of vitamin Dsubsequent to myocardial infarction can be attributed to an attenuation of theprocesses involved in inflammation, fibrosis, apoptosis, LV remodeling as well asanti-arrhythmic actions. The gene discussed is VDR; the disease is myocardial infarction.