AUTHOR=Burtenshaw Denise , Kitching Michael , Redmond Eileen M. , Megson Ian L. , Cahill Paul A. 

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

JOURNAL=Frontiers in Cardiovascular Medicine

VOLUME=6

YEAR=2019

URL=https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2019.00089

DOI=10.3389/fcvm.2019.00089

ISSN=2297-055X

ABSTRACT=<p>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 <italic>in-vivo</italic> 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.</p>