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(Circulation Research. 2008;103:907.)
© 2008 American Heart Association, Inc.

Editorials

Circulating Isoprostanes

Gate Keepers in the Route From Oxidative Stress to Vascular Dysfunction

Heinrich Sauer, Maria Wartenberg

From the Department of Physiology (H.S.), Justus Liebig University Giessen; and Department of Internal Medicine I (M.W.), Cardiology Division, Friedrich Schiller University Jena, Germany.

Correspondence to Prof Dr Heinrich Sauer, Department of Physiology, Justus Liebig University Giessen, Aulweg 129, 35392 Giessen, Germany. E-mail heinrich.sauer@physiology.med.uni-giessen.de

See related article, pages 1037–1046

Key Words: angiogenesis • oxidant signaling • oxidative stress • thromboxane

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

Through reading textbooks on pathophysiology, medical students already learn during their early university years that cardiovascular disease (CVD) is closely associated with oxidative stress, which apparently promotes progression of diseases like atherosclerosis, diabetes mellitus, hypertension, and ischemic heart disease. Oxidative stress is created through reactive oxygen species (ROS), eg, the superoxide anion and hydrogen peroxide, that are generated mainly within the mitochondrial respiratory chain or through activity of NADPH oxidases and reduce the bioavailability of nitric oxide (NO), which is the nodal point of endothelial vasomotor control and vascular function.¹ ROS are not only prooxidative reactive substances that alter the bioactivity of a variety of cellular molecules but are also known to regulate several classes of genes that are involved in the complex network of vascular growth and function, eg, formation of focal adhesion molecules, expression of metalloproteinases, cytokines and growth factors and, thus, when occurring in excessive amounts, may tilt the endothelial balance toward vasoconstriction and endothelial dysfunction. Furthermore, ROS can interfere with the plasma membrane phospholipid bilayer, which is easily prone to lipid peroxidation, thus resulting in the generation of a number of degradation products displaying potential detrimental bioactivity that may finally initiate vascular dysfunction. Over the last decade, a number of biomarkers of oxidative stress in vivo have been identified that caution against cardiovascular risk factors, the severity of CVD, and cardiovascular outcomes. Among these biomarkers of oxidative stress are a class of prostaglandin F₂–like compounds (F₂-isoprostanes [F₂-IsoPs]), which are generated from the nonenzymatic, . . . [Full Text of this Article]

Related Article:

Isoprostanes Inhibit Vascular Endothelial Growth Factor–Induced Endothelial Cell Migration, Tube Formation, and Cardiac Vessel Sprouting In Vitro, As Well As Angiogenesis In Vivo via Activation of the Thromboxane A₂ Receptor: A Potential Link Between Oxidative Stress and Impaired Angiogenesis

Ralf A. Benndorf, Edzard Schwedhelm, Anke Gnann, Raihana Taheri, Ghainsom Kom, Michael Didié, Anna Steenpass, Süleyman Ergün, and Rainer H. Böger
Circ. Res. 2008 103: 1037-1046. [Abstract] [Full Text] [PDF]

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