Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 301, Issue 3, Pages H647-H653Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.01271.2010
Keywords
reactive oxygen species; mitochondria; endothelial dysfunction
Funding
- National Heart, Lung, and Blood Institute [HL-080704, HL-094971]
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Zinkevich NS, Gutterman DD. ROS-induced ROS release in vascular biology: redox-redox signaling. Am J Physiol Heart Circ Physiol 301: H647-H653, 2011. First published June 17, 2011; doi:10.1152/ajpheart.01271.2010.-The involvement of reactive oxygen species (ROS) in regulating vascular function both in normal vessels and as part of an adaptive response during disease has been intensively studied. From the recognition that ROS serve as important signaling molecules has emerged multiple lines of evidence that there is a functional connectivity between intracellular sites of ROS production. This cross talk has been termed ROS-induced ROS release (RIRR) and is supported by a variety of observations showing that RIRR is a common mechanism for ROS amplification and regional ROS generation. The compartmentalization of ROS production within a cell is critical to its signaling function and is facilitated by microlocalization of specific scavengers. This review will provide descriptions and examples of important mechanisms of RIRR.
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