Reactive Oxygen Species (ROS), Intimal Thickening and Subclinical Atherosclerotic Disease
- 1Dublin City University, Ireland
- 2University of Rochester, United States
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 peroxidation. 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 (EndoMT). 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.
Keywords: NOX, NAPDH oxidase, Smooth muscle (physiology), Endothelial Cells, Adventitial cells, Stem Cells, Intimal thickening, Arteriosclerosis
Received: 21 Mar 2019;
Accepted: 14 Jun 2019.
Edited by:Abdelali Agouni, Qatar University, Qatar
Reviewed by:Jenny Jongstra-Bilen, University Health Network (UHN), Canada
Simona A. Manea, Institute of Cellular Biology and Pathology (ICBP), Romania
Copyright: © 2019 Kitching, Burtenshaw, Redmond and Cahill. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Prof. Paul A. Cahill, Dublin City University, Dublin, Dublin 9, County Dublin, Ireland, firstname.lastname@example.org