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Circulation Research. 2008;103:571-572
doi: 10.1161/CIRCRESAHA.108.184325
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(Circulation Research. 2008;103:571.)
© 2008 American Heart Association, Inc.


Editorials

Reactive Oxygen Species

Finding the Right Balance

Craig N. Morrell

From the Department of Molecular and Comparative Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, Md.

Correspondence to Craig N. Morrell, The Johns Hopkins University School of Medicine, Broadway Research Building, Suite 853, Baltimore, MD 21205. E-mail cmorrell@jhmi.edu



See related article, pages 598–605


Key Words: ROS • endothelial • inflammation • exocytosis • atherosclerosis


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


*    Introduction
 
Appropriate regulation of reactive oxygen species (ROS) has a significant impact on health and disease. ROS includes oxygen ions (O2·) free radicals (superoxide [OFormula ,2] and hydroxyl radicals), and peroxides (hydrogen peroxide [H2O2]) and are the products of normal oxygen consuming metabolic process in the body. ROS are small and highly reactive molecules with important cell signaling roles when maintained at proper cellular concentrations. During times of cell stress ROS levels can greatly increase. Because of their highly reactive nature, ROS can modify other oxygen species, proteins, or lipids, a situation often termed oxidative stress. Maintaining normal cellular ROS concentrations is, therefore, vital to the proper physiological function of numerous cell types throughout the body. An excess production or decreased scavenging of ROS has been implicated in the pathogenesis of diverse diseases such as neurodegeneration, diabetes, cancer, and atherosclerosis.

Kisucka et al now demonstrate that peroxiredoxin1 (Prdx1) has an important role in the maintenance of endothelial ROS.1 Prdx1 is an antioxidant enzyme that reduces H2O2, lipid peroxides, and peroxynitrite. Prior studies have shown that Prdx1–/– mice develop late onset hemolytic anemia and have increased frequency of cancer2 caused by an increase in ROS (such as H2O2), emphasizing the importance of Prdx1 in normal vascular homeostasis. Like many ROS, H2O2 can have disparate effects depending on the cell type and its local concentration. H2O2 can have normal regulatory functions as a second messenger molecule in signal transduction such as in the mitogen-activated . . . [Full Text of this Article]


Related Article:

Peroxiredoxin1 Prevents Excessive Endothelial Activation and Early Atherosclerosis
Janka Kisucka, Anil K. Chauhan, Ian S. Patten, Ayce Yesilaltay, Carola Neumann, Richard A. Van Etten, Monty Krieger, and Denisa D. Wagner
Circ. Res. 2008 103: 598-605. [Abstract] [Full Text] [PDF]