Reactive Oxygen Species in Pathogenesis of Atherosclerosis

Abstract

The volume of publications on the role of reactive oxygen species (ROS) in biological processes has been increasing exponentially over the last decades. ROS in large amounts clearly have detrimental effects on cell physiology, whereas low concentrations of ROS are permanently produced in cells and play a role as signaling molecules. An imbalance in ROS production and defense mechanisms can lead to pathological vascular remodeling, atherosclerosis being among them. The aim of this review is to examine different sources of ROS from the point of view of their participation in pathogenesis of atherosclerosis and related cardiovascular risk. Among the possible sources of ROS discussed here are mitochondria, NADPH-oxidases, xanthine oxidase, peroxidases, NO-synthases, cytochrome P450, cyclooxygenases, lipoxygenases, and hemoglobin of red blood cells. A great challenge for future research is to establish interrelations, feedback and feed-forward regulation mechanisms of various sources of ROS in development of atherosclerosis and other vascular pathologies.

Acetyl-11-Keto-β-Boswellic Acid Attenuates Prooxidant and Profibrotic Mechanisms Involving Transforming Growth Factor-β1, and Improves Vascular Remodeling in Spontaneously Hypertensive Rats

“…Oxidative damage plays a critical role in this process830. Gene transfer of catalase can reduce ROS production and ameliorate vascular remodeling, as is found31.…”

“…Although present agents control blood pressure well, the nontoxic agents for vasoprotection are weakly effective but still necessary. It has been proved that excessive reactive oxygen species (ROS) are closely related to vascular pathologies8. Vascular wall is particularly vulnerable to oxidative damage.…”

Probucol Protects Endothelial Progenitor Cells Against Oxidized Low-Density Lipoprotein via Suppression of Reactive Oxygen Species Formation In Vivo

“…Reactive oxygen species (ROS) plays a critical role in the development of atherosclerosis [25][26][27]. It was demonstrated that a significant amount of ROS was produced spontaneously from ox-LDL at clinically relevant concentrations, and was involved in the action of ox-LDL on human umbilical vein endothelial cells [28,29], bone marrow (BM) stem cells [30], vascular smooth muscle cells [31], monocytes [32], macrophage [33] and foam cells [34].…”

Action mechanism and cardiovascular effect of anthocyanins: a systematic review of animal and human studies

“…The most common cause of CVD is atherosclerosis, which involves inflammation in the vessel wall, as explained above [8]. It is frequently caused by the infiltration of low density lipoproteins (LDL) the endothelium through a wall damage, once trapped in the sub endothelium, the LDL became more prone forming the oxidized LDL (oxLDL) [9, 10].…”