Cellular electrophysiology and cardiac hypertrophy and heart failure regulation

Cardiovascular diseases remain the leading cause of death in developed countries. Last stage of cardiac pathologies, heart failure is major cause of morbidity and mortality. Despite therapeutic improve, heart failure patient’s prognostic is very poor, and more than 50% die suddenly as consequence of ventricular arrhythmia. This fact is the consequence of misunderstanding of the molecular mechanisms responsible of contractile dysfunction and arrhythmogenesis. It is thus imperative to elucidate the pathological mechanisms in order to find new therapeutic targets and develop efficient pharmacology.

Deficiency of vitamin D has been traditionally associated to rickets in children and osteomalacia and osteoporosis in adults. However, numerous observational and prospectives studies have shown that vitamin D deficiency may adversely affect both the risk of colorectal cáncer and several cardiovascular diseases, including heart failure. Moreover, deficiency of vitamin D is now recognized to be highly prevalent worldwide, particularly in the elderly population, impacting between 30% and 50% of the general population. Several randomized controlled clinical trial are in progress testing whether vitamin  D supplementation can reduce the risk of cardiovascular diseases, including progression of of left ventricular hypertrophy and development of heart failure.  The first results are expected by 2017.  However, the potential protective role of vitamin D in the heart, as well as the mechanism of action of the hormone in this organ, are poorly understood. Therefore, the aim of our project is to shed new light on the cellular and molecular mechanisms involved in the cardioprotective effects of vitamin D on heart failure.