Literature DB >> 17292046

Basic mechanisms of oxidative stress and reactive oxygen species in cardiovascular injury.

Christopher A Papaharalambus1, Kathy K Griendling.   

Abstract

The development of vascular disease has its origins in an initial insult to the vessel wall by biological or mechanical factors. The disruption of homeostatic mechanisms leads to alteration of the original architecture of the vessel and its biological responsiveness, contributing to acute or chronic diseases such as stroke, hypertension, and atherosclerosis. Endothelial dysfunction, macrophage infiltration of the vessel wall, and proliferation and migration of smooth muscle cells all involve different types of reactive oxygen species produced by various vessel wall components. Although basic science and animal research have clearly established the role of reactive oxygen species in the progression of vascular disease, the failure of clinical trials with antioxidant compounds has underscored the need for better antioxidant therapies and a more thorough understanding of the role of reactive oxygen species in cardiovascular physiology and pathology.

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Year:  2007        PMID: 17292046      PMCID: PMC1934425          DOI: 10.1016/j.tcm.2006.11.005

Source DB:  PubMed          Journal:  Trends Cardiovasc Med        ISSN: 1050-1738            Impact factor:   6.677


  59 in total

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Journal:  J Biol Chem       Date:  2003-09-04       Impact factor: 5.157

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  111 in total

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Review 6.  The importance of the endothelium in atherothrombosis and coronary stenting.

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7.  Oxidative inhibition of the vascular Na+-K+ pump via NADPH oxidase-dependent β1-subunit glutathionylation: implications for angiotensin II-induced vascular dysfunction.

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9.  A comparison of reactive oxygen species metabolism in the rat aorta and vena cava: focus on xanthine oxidase.

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10.  Erythroblast transformation-specific 2 correlates with vascular smooth muscle cell apoptosis in rat heterotopic heart transplantation model.

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