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Cited by 490

The DOI matches its Crossref record; 131 of the 131 references it cites were found in a registry or an index.

Oxidative stress and atherosclerosis

Open access
Singh, Uma, Jialal, Ishwarlal·2006·Pathophysiology
DOI 10.1016/j.pathophys.2006.05.002
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Abstract

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the Western world. Its incidence has been increasing lately in developing countries. Several lines of evidence support a role for oxidative stress in atherogenesis. Growing evidence indicates that chronic and acute overproduction of reactive oxygen species (ROS) under pathophysiologic conditions is integral in the development of cardiovascular diseases (CVD). ROS mediate various signaling pathways that underlie vascular inflammation in atherogenesis from the initiation of fatty streak development through lesion progression to ultimate plaque rupture. Various animal models of oxidative stress support the notion that ROS have a causal role in atherosclerosis and other cardiovascular diseases. Human investigations also support the oxidative stress hypothesis of atherosclerosis. Oxidative stress is the unifying mechanism for many CVD risk factors, which additionally supports its central role in CVD. A main source of ROS in vascular cells is the reduced nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase system. This is a membrane-associated enzyme, composed of five subunits, catalyzing the one-electron reduction of oxygen, using NADH or NADPH as the electron donor. This system is an important target for genetic investigations. Identification of groups of patients with genetically prone or resistant of oxidative stress is therefore an obvious target of investigation. A better understanding of the complexity of cellular redox reactions, development of a new class of antioxidants targeted to specific subcellular sites, and the phenotype-genotype linkage analysis for oxidative stress will likely be avenues for future research with regards to the broader use of pharmacological therapies in the treatment and prevention of CVD.

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Metadata

Authors
Singh, U., & Jialal, I.
Venue
Pathophysiology
Publisher
Elsevier BV
Published
2006-08
Volume
13
Issue
3
Pages
129-142
ISSN
0928-4680 (ISSN-L)
DOI
10.1016/j.pathophys.2006.05.002
OpenAlex
W2059350161
Cited by
490
References
131
FWCI
12.55
Type
journal article
Language
en
Open access
gold

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