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(Circulation Research. 2007;100:1128.)
© 2007 American Heart Association, Inc.

Reviews

Endothelial Mitochondria

Contributing to Vascular Function and Disease

Sean M. Davidson, Michael R. Duchen

From The Hatter Cardiovascular Institute (S.M.D.), Department of Medicine, Royal Free and University College Medical School, London; and Department of Physiology and the Mitochondrial Biology Group (M.R.D.), University College London, UK.

Correspondence to Sean M. Davidson, The Hatter Cardiovascular Institute, Department of Medicine, Royal Free and University College Medical School, 67 Chenies Mews, University College Hospital, London WC1E 6HX, United Kingdom. E-mail s.davidson{at}ucl.ac.uk

This Review is part of a thematic series on the 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

Defective Mitochondrial Biogenesis: A Hallmark of the High Cardiovascular Risk in Metabolic Syndrome?

Endothelial Mitochondria: Contributing to Vascular Function and Disease

Role of Mitochondria in Insulin Resistance
Marshall S. Runge Guest Editor

Disturbances in vascular function contribute to the development of several diseases of increasing prevalence and thereby contribute significantly to human mortality and morbidity. Atherosclerosis, diabetes, heart failure, and ischemia with attendant reperfusion injury share many of the same risk factors, among the most important being oxidative stress and alterations in the blood concentrations of compounds that influence oxidative stress, such as oxidized low-density lipoprotein. In this review, we focus on endothelial cells: cells in the frontline against these disturbances. Because ATP supplies in endothelial cells are relatively independent of mitochondrial oxidative pathways, the mitochondria of endothelial cells have been somewhat neglected. However, they are emerging as agents with diverse roles in modulating the dynamics of intracellular calcium and the generation of reactive oxygen species and nitric oxide. The mitochondria may also constitute critical "targets" of oxidative stress, because survival of endothelial cells can be compromised by opening of the mitochondrial permeability transition pore or by mitochondrial pathways of apoptosis. In addition, evidence suggests that endothelial mitochondria may play a "reconnaissance" role. For example, although the exact mechanism remains obscure, endothelial mitochondria may sense levels of oxygen in the blood and relay this information to cardiac myocytes as well as modulating the vasodilatory response mediated by endothelial nitric oxide.

Key Words: mitochondria • endothelial cells • intracellular calcium • reactive oxygen species • diabetes • atherosclerosis

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