doi: 10.1161/01.RES.0000248212.86638.e9
© 2006 American Heart Association, Inc.
Review |
Free Radicals, Mitochondria, and Oxidized Lipids
The Emerging Role in Signal Transduction in Vascular Cells
From the Department of Physiology and Biophysics (J.G.), Department of Pathology (S.W.B., V.M.D.-U., A.L.), and Center for Free Radical Biology (J.G., S.W.B., V.M.D.-U., A.L.), University of Alabama at Birmingham.
Correspondence to Aimee Landar, PhD, Biomedical Research Building II, 901 19th St S, Birmingham, AL 35294-2180. E-mail landar{at}uab.edu
This Review is part of a thematic series on Role of Mitochondria in Cardiovascular Diseases, which includes the following articles:
Free Radicals, Mitochondria, and Oxidized Lipids: The Emerging Role in Signal Transduction in Vascular Cells
Mitochondrial Dysfunction in Atherosclerosis
Mitochondrial Biology and Vascular Biology
Cardiac Mitochondriagenesis: An Adaptive or Maladaptive Phenomenon?
Role of Mitochondria in Insulin Resistance
Marschall S. Runge Guest Editor
Mitochondria have long been known to play a critical role in maintaining the bioenergetic status of cells under physiological conditions. It was also recognized early in mitochondrial research that the reduction of oxygen to generate the free radical superoxide occurs at various sites in the respiratory chain and was postulated that this could lead to mitochondrial dysfunction in a variety of disease states. Over recent years, this view has broadened substantially with the discovery that reactive oxygen, nitrogen, and lipid species can also modulate physiological cell function through a process known as redox cell signaling. These redox active second messengers are formed through regulated enzymatic pathways, including those in the mitochondrion, and result in the posttranslational modification of mitochondrial proteins and DNA. In some cases, the signaling pathways lead to cytotoxicity. Under physiological conditions, the same mediators at low concentrations activate the cytoprotective signaling pathways that increase cellular antioxidants. Thus, it is critical to understand the mechanisms by which these pathways are distinguished to develop strategies that will lead to the prevention of cardiovascular disease. In this review, we describe recent evidence that supports the hypothesis that mitochondria have an important role in cell signaling, and so contribute to both the adaptation to oxidative stress and the development of vascular diseases.
Key Words: apoptosis • atherosclerosis • hypertension • diabetes • environmental tobacco smoke • endothelial cells • electrophilic lipids • mitochondria • prostaglandins • redox signaling • thiols
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