Editorials |
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 |
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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
Related Article:
Circ. Res. 2008 103: 598-605.
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