Oxidative stress in chronic vascular disease: From prediction to prevention

Abstract This review article is intended to describe the strong relationship between oxidative stress and vascular disease. Reactive oxygen species (ROS) play an important role in the pathogenesis of vascular disease: oxidative stress is intimately linked to atherosclerosis, through oxidation of LDL...

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Published inVascular pharmacology Vol. 74; pp. 23 - 37
Main Authors Santilli, Francesca, D'Ardes, Damiano, Davì, Giovanni
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.11.2015
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Summary:Abstract This review article is intended to describe the strong relationship between oxidative stress and vascular disease. Reactive oxygen species (ROS) play an important role in the pathogenesis of vascular disease: oxidative stress is intimately linked to atherosclerosis, through oxidation of LDL and endothelial dysfunction, to diabetes, mainly through advanced glycation end-products (AGEs)/receptor for AGE (RAGE) axis impairment, protein kinase C (PKC), aldose reductase (AR) and NADPH oxidase (NOX) dysfunction, and to hypertension, through renin–angiotensin system (RAS) dysfunction. Several oxidative stress biomarkers have been proposed to detect oxidative stress levels and to improve our current understanding of the mechanisms underlying vascular disease. These biomarkers include ROS-generating and quenching molecules, and ROS-modified compounds, such as F2 -isoprostanes. An efficient therapeutic approach to vascular diseases cannot exclude evaluation and treatment of oxidative stress. In fact, oxidative stress represents an important target of several drugs and nutraceuticals, including antidiabetic agents, statins, renin-angiotensin system blockers, polyphenols and other antioxidants. A better understanding of the relations between atherosclerosis, diabetes, hypertension and ROS and the discovery of new oxidative stress targets will translate into consistent benefits for effective vascular disease treatment and prevention.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:1537-1891
1879-3649
DOI:10.1016/j.vph.2015.09.003