Editorials |
From the Division of Cardiology, Department of Medicine, Emory University School of Medicine, and the Atlanta Veterans Affairs Medical Center, Atlanta, Ga.
Correspondence to W. Robert Taylor, MD, PhD, 1639 Pierce Dr. WMB 319, Atlanta, GA 30322. E-mail wtaylor@emory.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Over the last decade, there has been a growing body of evidence defining the importance of reactive oxygen species (ROS) in the development of cardiovascular diseases. In blood vessels, ROS have not only been found to be involved in pathologic processes like hypertension, atherosclerosis, restenosis, and diabetic vascular disease, but they also have been shown to work as intracellular messengers that regulate several physiological mechanisms, such as modulation of vessel tone, vascular smooth muscle cell (VSMC) and endothelial cell (EC) apoptosis, VSMC proliferation, hypertrophy, and migration.1 The level of ROS in cells depends on a delicate balance between their production and destruction. A major source of ROS in VSMCs is the NADPH oxidase,2 but other sources like complex III of the electron transport chain in mitochondria may play an important role in their production.3,4
See page 950
As a result of its short half life (
104 seconds), its low diffusivity through lipid membranes, and its ability to quickly react with NO to produce perxinitrite (ONOO), superoxide is the most likely ROS to have distinct effects depending on its subcelullar localization. Moreover, VSMCs produce several different superoxide scavenger enzymes located in different areas of the cell: SOD1 (Cu/ZnSOD), which accounts for 50% to 80% of total SOD in blood vessels and is localized primarily in the cytosol and nucleus5; SOD2 (MnSOD), expressed in smaller quantities in VSMCs, more abundantly in ECs, and localized to the mitochondria5; and SOD3 (ecSOD) which is bound to the cell membrane through
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Arterioscler Thromb Vasc Biol 2005 25: 950-956.
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