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PII S1050-1738(01)00096-2 TCM
NAD(P)H Oxidases and Their
Relevance to Atherosclerosis
Dan Sorescu, Katalin Szöcs, and Kathy K. Griendling*
Studies performed during the last decade have identiﬁed NAD(P)H oxi-
dases unique to nonphagocytic vascular cells. The reactive oxygen spe-
cies 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 impor-
tant determinants of the course of vascular disease. (Trends Cardio-
vasc Med 2001;11:124–131). © 2001, Elsevier Science Inc.
Basic physiological cellular processes
such as growth, migration, senescence
and apoptosis are controlled by coordi-
nated molecular signaling events. Until
recently, it was perceived that these mo-
lecular switches are primarily proteins,
lipids, or a combination of these, which
assemble dynamically in complex struc-
tures to amplify and transmit signals to
different intracellular effectors. Recently,
however, this central dogma has been
challenged by the fundamental discov-
ery that very simple chemical molecules
such as superoxide (O
), nitric oxide
), hydrogen peroxide (H
) or per-
), classiﬁed as reactive
oxygen species (ROS), can also function
as second messengers for the traditional
kinase/phosphatase systems, thus inﬂu-
encing fundamental physiological and
pathological processes. Therefore, it has
become increasingly important to charac-
terize the source, location, mechanism of
action and the target molecules for ROS.
This review article focuses mainly on
the vascular NAD(P)H oxidases as an en-
zymatic source of O
their potential relevance to atherogenesis.
Dan Sorescu, Katalin Szöcs, and Kathy K.
Griendling are from the Division of Cardiol-
ogy, Department of Medicine, Emory Univer-
sity, Atlanta, Georgia.
* Address correspondence to: Kathy K.
Griendling, Emory University, Division of
Cardiology, 319 WMB, 1639 Pierce Dr.,
Atlanta, GA 30322, USA. Tel.: 404-727-8386;
fax: 404-727-3585; e-mail: email@example.com.
© 2001, Elsevier Science Inc. All rights
reserved. 1050-1738/01/$-see front matter