Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2082966 | Drug Discovery Today: Therapeutic Strategies | 2008 | 9 Pages |
Abstract
Oxidant stress has been implicated in the etiology and pathogenesis of atherothrombotic vascular disease. Elevated levels of reactive oxygen species, resulting from increased production and/or decreased antioxidant capacity, modulate the vessel wall phenotype to create an environment that facilitates the progression of atherosclerosis. Herein, we review a number of biochemical mechanisms by which oxidant stress mediates atherosclerotic lesion formation and progression.
Section editors:Colin H. Macphee – Department of Vascular Biology, GlaxoSmithKline, King of Prussia, PA, USAAlan Daugherty – Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Biotechnology
Authors
Jane A. Leopold, Joseph Loscalzo,