Circulation Research. 2006;98:453-462
doi: 10.1161/01.RES.0000204727.46710.5e
doi: 10.1161/01.RES.0000204727.46710.5e
© 2006 American Heart Association, Inc.
Reviews |
Regulation of NADPH Oxidases
The Role of Rac Proteins
From the Department Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, The Netherlands.
Correspondence to Peter L. Hordijk, Department Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Plesmanlaan 125, 1066 CX Amsterdam, The Netherlands. E-mail p.hordijk{at}sanquin.nl
This Review is part of a thematic series on The Role of Small GTPases in Cardiovascular Biology, which includes the following articles:
Rho GTPases, Statins and NO: The Role of Small GTPases in Endothelial Cytoskeletal Dynamics and the Sheer Stress Response
Rho Kinases in Cardiovascular Physiology and Pathophysiology
Regulation of NADPH Oxidases: The Role of Rac Proteins
Rho GTPases and Signaling by Endothelial Receptors
The Rac and Rho Hall of Fame: A Decade of Hypertrophic Signaling Hits
Anne Ridley Guest Editor
The role for reactive oxygen species (ROS) in cellular (patho)physiology, in particular in signal transduction, is increasingly recognized. The family of NADPH oxidases (NOXes) plays an important role in the production of ROS in response to receptor agonists such as growth factors or inflammatory cytokines that signal through the Rho-like small GTPases Rac1 or Rac2. The phagocyte oxidase (gp91phox/NOX2) is the best characterized family member, and its mode of activation is relatively well understood. Recent work has uncovered novel and increasingly complex modes of control of the NOX2-related proteins. Some of these, including NOX2, have been implicated in various aspects of (cardio)vascular disease, including vascular smooth muscle and endothelial cell hypertrophy and proliferation, inflammation, and atherosclerosis. This review focuses on the role of the Rac1 and Rac2 GTPases in the activation of the various NOX family members.
Key Words: NADPH oxidase • Rac1 • reactive oxygen species
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