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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:703.)
© 2007 American Heart Association, Inc.

Editorials

All Oxidase Roads Lead to Angiotensin, Too

Lilach O. Lerman; Amir Lerman

From the Divisions of Nephrology and Hypertension (L.O.L.) and Cardiovascular Diseases (L.O.L., A.L.) Mayo Clinic College of Medicine, Rochester, Minn.

Correspondence to Amir Lerman, MD, Division of Cardiovascular Diseases Mayo Clinic Rochester 200 First Street SW, Rochester, MN 55905. E-mail lerman.amir@mayo.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Free radicals and other oxygen- or nitrogen-derived reactive species formed during cellular metabolism and respiration, like superoxide (O₂^·–), hydrogen peroxide (H₂O₂), and nitric oxide (NO), are important second messengers and fundamental mediators in biological processes, redox signaling, and cellular growth. However, over the past 2 decades it has become clear that reactive oxygen species (ROS) in particular are also important participants in a number of pathological processes, including cardiovascular and kidney diseases. In fact, increased production of ROS has been proposed as a common pathomechanism by which cardiovascular risk factors affect the vessel wall to induce and amplify vessel and organ injury.

See page 943

Several possible enzymatic sources of ROS have been identified in blood vessels and other tissues, such as nicotineamide adenine dinucleotide (phosphate) oxidase (NAD(P)H oxidase), xanthine oxidase (XO), and uncoupled nitric oxide synthase. NAD(P)H oxidase has long been considered one of the most important sources of ROS in the vessel wall. One of its most potent stimulants is angiotensin II. In turn, NAD(P)H oxidase mediates several downstream effects of angiotensin II like inflammation, endothelial dysfunction, collagen deposition, and vascular hypertrophy.

Nevertheless, an important role in the pathogenesis of cardiovascular disease has also been ascribed to XO. This ROS-producing enzyme is generated by the posttranslational modification of xanthine dehydrogenase, catalyzes the oxidation of purines to uric acid, and in the process reduces molecular oxygen and generates the free radical superoxide (Figure). In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Landmesser . . . [Full Text of this Article]

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Angiotensin II Induces Endothelial Xanthine Oxidase Activation: Role for Endothelial Dysfunction in Patients With Coronary Disease

Ulf Landmesser, Stephan Spiekermann, Christoph Preuss, Sajoscha Sorrentino, Dieter Fischer, Costantina Manes, Maja Mueller, and Helmut Drexler
Arterioscler Thromb Vasc Biol 2007 27: 943-948. [Abstract] [Full Text] [PDF]

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