Oxidant stress in atherosclerosis: Oxidatively modified LDL and LOX-1

Abstract

Oxidative stress, implying an imbalance between oxidant and anti-oxidant species, is present in the atherosclerotic regions and plays a significant role in the pathogenesis of atherosclerosis and its complications. Recent studies have demonstrated an association between increased oxidative stress and diabetes, hypertension, cigarette smoking and dyslipidemia, which are well known risk factors for atherosclerosis. The endothelial cells, the primary cell line to become dysfunctional early in the course of atherosclerosis internalizes ox-LDL mainly through its receptor LOX-1 which is responsible for many of the downstream effects on smooth muscle cell ans monocyte biology. Inhibition of LOX-1 by gene deletion significantly reduces atherogenesis in animal models. Many of the currently used drugs modulate atherosclerosis by their action on LOX-1 receptor. New molecules that modulate LOX-1 are currently under investigation. sLOX-1 is a potential biomarker in acute coronary injury and further studies needs to be done before it can be put to clinical use.