Reactive Oxygen Species (ROS), Intimal Thickening, and Subclinical Atherosclerotic Disease

Abstract

Arteriosclerosis causes significant morbidity and mortality worldwide. Central to this process is the development of subclinical non-atherosclerotic intimal lesions before the appearance of pathologic intimal thickening and advanced atherosclerotic plaques. Intimal thickening is associated with several risk factors, including oxidative stress due to reactive oxygen species (ROS), inflammatory cytokines and lipid. The main ROS producing systems in-vivo are reduced nicotinamide dinucleotide phosphate (NADPH) oxidase (NOX). ROS effects are context specific. Exogenous ROS induces apoptosis and senescence, whereas intracellular ROS promotes stem cell differentiation, proliferation, and migration. Lineage tracing studies using murine models of subclinical atherosclerosis have revealed the contributory role of medial smooth muscle cells (SMCs), resident vascular stem cells, circulating bone-marrow progenitors and endothelial cells that undergo endothelial-mesenchymal-transition (EndMT). This review will address the putative physiological and patho-physiological roles of ROS in controlling vascular cell fate and ROS contribution to vascular regeneration and disease progression.

Essential Role of Nonessential Amino Acid Glutamine in Atherosclerotic Cardiovascular Disease

“…Recent studies showed that ROS increases the pyroptosis of VEC that contributes to VEC dysfunction and As progression (Wu et al, 2018;Zhaolin et al, 2019). Lowering oxidative stress injury induced by ROS is considered as a promising therapy to inhibit the progression of As (Burtenshaw et al, 2019).…”

Oxidative stress and inflammation in the development of cardiovascular disease and contrast induced nephropathy

“…Vascular NOXs are important ROS generating enzymes and in human vascular cells, NOX1, NOX2, NOX4 and NOX5 are expressed. NOX are transmembrane enzyme complexes with a few regulatory subunits and a core catalytic subunit, except for NOX5 [111] . NOX activation results in the generation of O 2 from molecular oxygen by the transfer of electrons from NADPH [112] .…”

“…NADPH oxidase in humans was thought to be phagocyte specific as the two membrane bound units, gp91 phox and p22 phox form a heterodimer and mediate bacterial killing by generating O 2 (gp91 phox produces a burst of O 2 and p22 phox acts to stabilize gp91 phox , enhancing O 2 production) [113] . P22 phox expression in non-phagocytic cells directed the discovery of NOX1 in non-phagocytic cells which then led to the identification of the other NOX proteins [111] .…”

Combined Extract of Vitis vinifera L. and Centella asiatica Synergistically Attenuates Oxidative Damage Induced by Hydrogen Peroxide in Human Umbilical Vein Endothelial Cells

“…The vascular endothelium plays a pivotal role in vascular permeability, maintenance of vascular tone and pressure, platelet aggregation, and thrombosis (Minami et al, 2019). Endothelial cells can be easily damaged by various factors, such as inflammatory cytokines and reactive oxygen species (ROS), which cause endothelial dysfunction that, in turn, initiate early processes of vascular diseases, including atherosclerosis, hypertension, and peripheral venous disease (Herrera et al, 2010;Burtenshaw et al, 2019).…”