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

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 seve...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in cardiovascular medicine Vol. 6; p. 89
Main Authors Burtenshaw, Denise, Kitching, Michael, Redmond, Eileen M., Megson, Ian L., Cahill, Paul A.
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 02.08.2019
Subjects
adventitial cells
Cardiovascular Medicine
endothelial cells
NAPDH oxidase
NOX
smooth muscle (physiology)
stem cells
stem cells
arteriosclerosis
endothelial cells
NAPDH oxidase
NOX
intimal thickening
smooth muscle (physiology)
adventitial cells
Online AccessGet full text

Cover

More Information
Summary: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 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.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
This article was submitted to Cardiovascular Biologics and Regenerative Medicine, a section of the journal Frontiers in Cardiovascular Medicine
These authors have contributed equally to this work
Edited by: Abdelali Agouni, Qatar University, Qatar
Reviewed by: Jenny Jongstra-Bilen, University Health Network (UHN), Canada; Simona Adriana Manea, Institute of Cellular Biology and Pathology (ICBP), Romania
ISSN:2297-055X
2297-055X
DOI:10.3389/fcvm.2019.00089