Abstract
Atherosclerosis can be regarded as chronic inflammatory disease affecting the arterial wall. Despite the recent progress in studying the pathogenesis of atherosclerosis, some of the pathogenic mechanisms remain to be fully understood. Among these mechanisms is oxidative stress, which is closely linked to foam cells formation and other key events in atherosclerosis development. Two groups of enzymes are involved in the emergence of oxidative stress: Pro-oxidant (including NADPH oxidases, xanthine oxidases, and endothelial nitric oxide synthase) and antioxidant (such as superoxide dismutase, catalases, and thioredoxins). Pro-oxidant enzymes in normal conditions produce moderate concentrations of reactive oxidant species that play an important role in cell functioning and can be fully utilized by antioxidant enzymes. Under pathological conditions, activities of both pro-oxidant and antioxidant enzymes can be modified by numerous factors that can be relevant for developing novel therapies. Recent studies have explored potential therapeutic properties of antioxidant molecules that are capable to eliminate oxidative damage. However, the results of these studies remain controversial. Other perspective approach is to inhibit the activity of pro-oxidant enzymes and thus to slow down the progression of atherosclerosis. In this review we summarized the current knowledge on oxidative stress in atherosclerosis and potential antioxidant approaches. We discuss several important antioxidant molecules of plant origin that appear to be promising for treatment of atherosclerosis.
Highlights
Oxidative stress was first defined in 1985 by Helmut Sies as “a disturbance in the pro-oxidant to antioxidant balance in favor of the oxidant species, leading to potential damage”
Upregulation of SODs does not lead to the reduction of ROS production directly, because of the high amounts of distal oxidants produced from hydrogen peroxide, that contribute to the atherosclerosis development
Study by Ma et al revealed that melatonin can promote ROS scavenging by mitophagy in macrophages within and to suppress prolonged NLRP3 inflammasome activation in atherosclerotic lesions, which resulted in attenuation of atherosclerosis progression in apoE-/- mice fed a high-fat diet [93]
Summary
Oxidative stress was first defined in 1985 by Helmut Sies as “a disturbance in the pro-oxidant to antioxidant balance in favor of the oxidant species, leading to potential damage”. Introduction of this concept resulted in the development of a new research area named Redox Biology [1,2]. The modern concept of oxidative stress includes more details: “the lack of balance between the occurrence of reactive oxygen/nitrogen species (ROS/RNS) and the capacity of organism to counteract their action by the antioxidative protection systems” [3]. Mitochondrial oxidative stress can occur due to excessive ROS production or failure of antioxidant mechanisms. The protective effect of vitamin E for prevention of cancer and major cardiovascular outcomes could not be proven [11]
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