Rheumatic heart disease (RHD) remains a major cause of cardiac related mortality and morbidity in the developing countries due to poor diagnosis and lack of proper
therapeutics. The definite reason of heart valve injury during RHD is poorly understood. Valvular endothelial cells play an important role in pathogenesis of different
cardiovascular diseases. Besides, the regulation of
vitamin D (calciferol) and
VEGF (
vascular endothelial growth factor) results in the functional changes in endothelial cells. However, the crosstalk between
vitamin D and
VEGF in the pathogenesis of RHD is not yet unfurled. Evidences in the concerned fields are documented by searching through Google Scholar and Pubmed. Literature based survey has revealed that vascular endothelium, especially endothelial cells play important roles in valvular remodelling during
cardiovascular diseases. Endothelial cell dysfunction leads to heart valve remodelling, which furthermore initiates the pathogenesis of
valvular heart disease.
Vitamin D has the potential to maintain the concentration of
VEGF in the circulation and induce the function of endothelial cells. Hence, we hypothesize that
vitamin D and
VEGF homeostasis can alter the function of endothelial cells, which may subsequently trigger the valvular remodelling or even damage of heart valves during the progression of RHD pathogenesis. Our hypothesis shed light on the evidence based knowledge translation of plausible cellular phenomena due to
vitamin D/
VEGF homeostasis during valvular vandalism in RHD.