TY - JOUR
T1 - Redox control of vascular smooth muscle proliferation
AU - Griendling, Kathy K.
AU - Ushio-Fukai, Masuko
N1 - Funding Information:
he generation of oxygen-derived free radicals is often considered to be toxic to cells. Recently, T however, it has become apparent that in some systems, free radicals such as -0 2-are actually growth promoting. The most well-studied example is tumor promotion. 10xidase activity and abnormalities in oxygen metabolism have been shown to be related to growth in tumor cells. 1 In fact, four different types of antitumor agents also inhibit the plasma membrane redox system, 1 implying that the redox state of the cell may be a common step at which growth control can be From Emory University School of Medicine, Division of CardiologY. Supported by National Institutes of Health Grants HL38206 and HL58863. Submitted for publication June 27, 1997; revision submitted Sept. 3, 1997; accepted Sept. 11, 1997. Reprint requests: Kathy K. Griendling, PhD, Emory University School of Medicine, Division of Cardiology, 319 Woodruff Memorial Building, 1639 Pierce Drive, Atlanta, GA 30322. Copyright © 1998 by Mosby, Inc. 0022-2143/98 $5.00 + 0 5/1/90339 achieved. Because many cardiovascular diseases are accompanied by abnormal VSMC growth, this concept is particularly relevant to the cardiovascular system. This review will summarize the evidence for redox control of vascular growth and discuss the possible molecular mechanisms involved.
PY - 1998/7
Y1 - 1998/7
N2 - 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.
AB - 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.
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U2 - 10.1016/S0022-2143(98)90019-1
DO - 10.1016/S0022-2143(98)90019-1
M3 - Review article
C2 - 9665366
AN - SCOPUS:0032126920
SN - 0022-2143
VL - 132
SP - 9
EP - 15
JO - Journal of Laboratory and Clinical Medicine
JF - Journal of Laboratory and Clinical Medicine
IS - 1
ER -