Research ExplorerPublicationsNAD(P)H oxidases and their relevance to atherosclerosis

NAD(P)H oxidases and their relevance to atherosclerosis

Standard

NAD(P)H oxidases and their relevance to atherosclerosis. / Sorescu, D; Szöcs, K; Griendling, K K.

In: TRENDS CARDIOVAS MED, Vol. 11, No. 3-4, 01.11.2001, p. 124-131.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Sorescu, D, Szöcs, K & Griendling, KK 2001, 'NAD(P)H oxidases and their relevance to atherosclerosis', TRENDS CARDIOVAS MED, vol. 11, no. 3-4, pp. 124-131. https://doi.org/10.1016/s1050-1738(01)00097-4

APA

Sorescu, D., Szöcs, K., & Griendling, K. K. (2001). NAD(P)H oxidases and their relevance to atherosclerosis. TRENDS CARDIOVAS MED, 11(3-4), 124-131. https://doi.org/10.1016/s1050-1738(01)00097-4

Vancouver

Sorescu D, Szöcs K, Griendling KK. NAD(P)H oxidases and their relevance to atherosclerosis. TRENDS CARDIOVAS MED. 2001 Nov 1;11(3-4):124-131. https://doi.org/10.1016/s1050-1738(01)00097-4

Bibtex

@article{71f83db00acd402a81da150f086cbeb8,
title = "NAD(P)H oxidases and their relevance to atherosclerosis",
abstract = "Studies performed during the last decade have identified NAD(P)H oxidases unique to nonphagocytic vascular cells. The reactive oxygen species released from these enzymes regulate fundamental cellular functions such as growth (hyperplastic or hypertrophic), endothelial dysfunction, migration and inflammation, which have been demonstrated to play a role in atherogenesis. Evidence from experimental animal and human studies implicate the nonphagocytic NAD(P)H oxidases in multiple aspects of atherogenesis, suggesting that these enzymes may be important determinants of the course of vascular disease.",
keywords = "Animals, Arteriosclerosis/enzymology, Endothelium, Vascular/enzymology, Humans, NADH, NADPH Oxidoreductases/metabolism, NADPH Oxidases, Oxidative Stress/physiology, Reactive Oxygen Species/metabolism",
author = "D Sorescu and K Sz{\"o}cs and Griendling, {K K}",
year = "2001",
month = nov,
day = "1",
doi = "10.1016/s1050-1738(01)00097-4",
language = "English",
volume = "11",
pages = "124--131",
journal = "TRENDS CARDIOVAS MED",
issn = "1050-1738",
publisher = "Elsevier Inc.",
number = "3-4",

}

RIS

TY - JOUR

T1 - NAD(P)H oxidases and their relevance to atherosclerosis

AU - Sorescu, D

AU - Szöcs, K

AU - Griendling, K K

PY - 2001/11/1

Y1 - 2001/11/1

N2 - Studies performed during the last decade have identified NAD(P)H oxidases unique to nonphagocytic vascular cells. The reactive oxygen species released from these enzymes regulate fundamental cellular functions such as growth (hyperplastic or hypertrophic), endothelial dysfunction, migration and inflammation, which have been demonstrated to play a role in atherogenesis. Evidence from experimental animal and human studies implicate the nonphagocytic NAD(P)H oxidases in multiple aspects of atherogenesis, suggesting that these enzymes may be important determinants of the course of vascular disease.

AB - Studies performed during the last decade have identified NAD(P)H oxidases unique to nonphagocytic vascular cells. The reactive oxygen species released from these enzymes regulate fundamental cellular functions such as growth (hyperplastic or hypertrophic), endothelial dysfunction, migration and inflammation, which have been demonstrated to play a role in atherogenesis. Evidence from experimental animal and human studies implicate the nonphagocytic NAD(P)H oxidases in multiple aspects of atherogenesis, suggesting that these enzymes may be important determinants of the course of vascular disease.

KW - Animals

KW - Arteriosclerosis/enzymology

KW - Endothelium, Vascular/enzymology

KW - Humans

KW - NADH, NADPH Oxidoreductases/metabolism

KW - NADPH Oxidases

KW - Oxidative Stress/physiology

KW - Reactive Oxygen Species/metabolism

U2 - 10.1016/s1050-1738(01)00097-4

DO - 10.1016/s1050-1738(01)00097-4

M3 - SCORING: Review article

C2 - 11686001

VL - 11

SP - 124

EP - 131

JO - TRENDS CARDIOVAS MED

JF - TRENDS CARDIOVAS MED

SN - 1050-1738

IS - 3-4

ER -