Furthermore, chronic exposure of endothelial cells to Hcy accelerated the rate of cellular senescence through the redox pathway suggesting that oxidative stress could increase the production of vascular cell senescence proven by increased expression of two surface molecules such as intracellular adhesion molecule-1 (ICAM-1) and plasminogen activator inhibitor-1 (PAI-1), factors implicated in the pathogenesis of atherosclerosis [73]. Here, SERPINE1 is linked to atherosclerosis.