Cardiovascular Diseases and Zinc

Abstract

Zinc is structurally and functionally essential for more than 300 enzymes and 2000 transcription factors in human body. Intracellular labile zinc is the metabolically effective zinc and tiny changes in its concentrations significantly affect the intracellular signaling and enzymatic responses. Zinc is crucial for the embrionic and fetal development of heart. Therefore, it is shown to be related with a variety of congenital heart defects. It is involved in epithelial-to-mesenchymal transformation including endocardial cushion development, which is necessary for atrioventricular septation as well as the morphogenesis of heart valves. In atherosclerosis, monocyte endothelial adhesion, and diapedesis, activation and transformation into macrophages and forming foam cells by the ingestion of oxidized LDL are monocyte related steps which need zinc. Intracellular zinc increases intracellular calcium through a variety of pathways and furthermore, zinc itself can work as a second messenger as calcium. These demonstrate the significance of intracellular zinc in heart failure and arterial hypertension. However, extracellular zinc has an opposite effect by blocking calcium channels, explaining decreased serum zinc levels, contrary to the increased cardiomyocyte and erythrocyte zinc levels in hypertensive subjects. These and other data in the literature demonstrate that zinc has important roles in healthy and diseased cardiovascular system but zinc-cardiovascular system relationship is so complex that, it has not been explained in all means. In this article, we try to review some of the available knowledge about this complex relationship.