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Abstract
Recent evidence suggests a role for reactive oxygen species in the control of vascular
smooth muscle proliferation both in vitro and in vivo. Oxidative stress increases
cell proliferation, mediates hormone-induced hypertrophy, and—under some circumstances—induces
apoptosis. Smooth muscle cells contain a reduced nicotinamide adenine dinucleotide/reduced
nicotinamide adenine dinucleotide phosphate oxidase that is responsible for the majority
of the superoxide produced by the vessel wall. This enzyme has been characterized
biochemically, but only limited information is available regarding its molecular structure.
High levels of oxidative stress are apparently involved in the pathogenesis of vascular
diseases such as hypertension and atherosclerosis, along with abnormal vascular growth
after balloon injury. Thus the pathways responsible for oxidative stress, as well
as the antioxidant defenses in the vessel wall, may provide novel therapeutic targets.
Abbreviations:
MAP kinase (mitogen-activated protein kinase), NADH (reduced nicotinamide adenine dinucleotide), NADPH (reduced nicotinamide adenine dinucleotide phosphate), O2− (superoxide), VSMC (vascular smooth muscle cell)To read this article in full you will need to make a payment
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Ushio-Fukai M, Alexander RW; Akers M; Griendling KK. p38 Mitogen-activated protein kinase is a critical component of the redox-sensitive signaling pathways activated by angiotensin II: role in vascular smooth muscle cell hypertrophy. J Bilo Chem. In press.
Article info
Publication history
Accepted:
September 11,
1997
Received in revised form:
September 3,
1997
Received:
June 27,
1997
Footnotes
☆Supported by National Institutes of Health Grants HL38206 and HL58863.
Identification
Copyright
© 1998 Published by Elsevier Inc.
