NAD(P)H oxidase-derived reactive oxygen species as mediators of angiotensin II signaling
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NAD(P)H oxidase-derived reactive oxygen species as mediators of angiotensin II signaling. / Hanna, Ibrahim R; Taniyama, Yoshihiro; Szöcs, Katalin; Rocic, Petra; Griendling, Kathy K.
in: ANTIOXID REDOX SIGN, Jahrgang 4, Nr. 6, 12.2002, S. 899-914.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - NAD(P)H oxidase-derived reactive oxygen species as mediators of angiotensin II signaling
AU - Hanna, Ibrahim R
AU - Taniyama, Yoshihiro
AU - Szöcs, Katalin
AU - Rocic, Petra
AU - Griendling, Kathy K
PY - 2002/12
Y1 - 2002/12
N2 - Angiotensin II has been shown to participate in both physiological processes, such as sodium and water homeostasis and vascular contraction, and pathophysiological processes, including atherosclerosis and hypertension. The effects of this molecule on vascular tissue are mediated at least in part by the modification of the redox milieu of its target cells. Angiotensin II has been shown to activate the vascular NAD(P)H oxidase(s) resulting in the production of reactive oxygen species, namely superoxide and hydrogen peroxide. In this article, we review what is known about the molecular steps that link angiotensin II and its receptor to production of reactive oxygen species and subsequent redox-mediated events, focusing on the structural and functional properties of the vascular NAD(P)H oxidases and their downstream mediators. As such, we provide a framework linking angiotensin II to crucial vascular pathologies, such as hypertension, atherosclerosis, and restenosis after angioplasty, by means of the NAD(P)H-dependent oxidases and their effector molecules.
AB - Angiotensin II has been shown to participate in both physiological processes, such as sodium and water homeostasis and vascular contraction, and pathophysiological processes, including atherosclerosis and hypertension. The effects of this molecule on vascular tissue are mediated at least in part by the modification of the redox milieu of its target cells. Angiotensin II has been shown to activate the vascular NAD(P)H oxidase(s) resulting in the production of reactive oxygen species, namely superoxide and hydrogen peroxide. In this article, we review what is known about the molecular steps that link angiotensin II and its receptor to production of reactive oxygen species and subsequent redox-mediated events, focusing on the structural and functional properties of the vascular NAD(P)H oxidases and their downstream mediators. As such, we provide a framework linking angiotensin II to crucial vascular pathologies, such as hypertension, atherosclerosis, and restenosis after angioplasty, by means of the NAD(P)H-dependent oxidases and their effector molecules.
KW - Angiotensin II/metabolism
KW - Animals
KW - Blood Vessels/enzymology
KW - Endothelium, Vascular/metabolism
KW - Humans
KW - Kidney Diseases/metabolism
KW - Muscle, Smooth, Vascular/enzymology
KW - NADPH Oxidases/metabolism
KW - Oxidation-Reduction
KW - Protein Kinases/metabolism
KW - Reactive Oxygen Species/metabolism
KW - Signal Transduction/physiology
KW - Transcription Factors/metabolism
KW - Vascular Diseases/metabolism
U2 - 10.1089/152308602762197443
DO - 10.1089/152308602762197443
M3 - SCORING: Journal article
C2 - 12573139
VL - 4
SP - 899
EP - 914
JO - ANTIOXID REDOX SIGN
JF - ANTIOXID REDOX SIGN
SN - 1523-0864
IS - 6
ER -