A Mechanistic Study of Endothelial Dysfunction and Cellular Senescence in Cardiovascular Disease

Abstract

Plasma concentrations of asymmetric dimethylarginine (ADMA), homocysteine (HCY) and s-adenosylhomocysteine (SAH) are well-established cardiovascular risk factors. Besides, these analytes have a critical role in influencing the diseases associated with elevated oxidative stress (OS) such as diabetes, hypertension and certain cancers. Interestingly, SAH is an endogenous inhibitor of a group of enzymes, methyltransferases (MTs), which are involved in the biosynthesis of ADMA. In this regard, logically, when SAH levels are elevated, due to its MT inhibitory effect, ADMA levels should be compromised. However, in coronary artery disease (CAD), there is an elevation of ADMA, HCY and SAH. This suggests that there could a mechanism which over-rides the inhibitory effect of SAH, which causes ADMA elevation newline