TY - JOUR
T1 - Reactive oxygen species as mediators of signal transduction in cardiovascular disease
AU - Abe, Jun Ichi
AU - Berk, Bradford C.
N1 - Copyright:
Copyright 2004 Elsevier Science B.V., Amsterdam. All rights reserved.
PY - 1998/2
Y1 - 1998/2
N2 - Reduction-oxidation (redox) reactions that generate reactive oxygen species (ROS) have been identified as important chemical processes that regulate signal transduction. Because increased ROS may be a risk factor for cardiovascular events such as unstable angina, myocardial infarction and sudden death, understanding the biological processes that generate ROS and the intracellular signals elicited by ROS will be important to gain insight into the pathogenesis of these diseases. In this review, we discuss the enzymes that generate ROS in cardiovascular tissues, the role of the mitogen- activated protein (MAP) kinase pathway in redox-sensitive signal transduction, and focus on tyrosine kinases as proximate 'sensors' for redox- mediated signal events. The mechanisms by which these kinases regulate gene transcription are then discussed to provide insight into the pathogenic roles of ROS in hypertension, atherosclerosis and vascular remodeling.
AB - Reduction-oxidation (redox) reactions that generate reactive oxygen species (ROS) have been identified as important chemical processes that regulate signal transduction. Because increased ROS may be a risk factor for cardiovascular events such as unstable angina, myocardial infarction and sudden death, understanding the biological processes that generate ROS and the intracellular signals elicited by ROS will be important to gain insight into the pathogenesis of these diseases. In this review, we discuss the enzymes that generate ROS in cardiovascular tissues, the role of the mitogen- activated protein (MAP) kinase pathway in redox-sensitive signal transduction, and focus on tyrosine kinases as proximate 'sensors' for redox- mediated signal events. The mechanisms by which these kinases regulate gene transcription are then discussed to provide insight into the pathogenic roles of ROS in hypertension, atherosclerosis and vascular remodeling.
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U2 - 10.1016/S1050-1738(97)00133-3
DO - 10.1016/S1050-1738(97)00133-3
M3 - Review article
C2 - 21235913
AN - SCOPUS:0031882260
SN - 1050-1738
VL - 8
SP - 59
EP - 64
JO - Trends in Cardiovascular Medicine
JF - Trends in Cardiovascular Medicine
IS - 2
ER -