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Role of Oxidative Modifications in Atherosclerosis

Centre for Vascular Research, University of New South Wales, and Department of Haematology, Prince of Wales Hospital, Sydney, New South Wales, Australia; and Whitaker Cardiovascular Institute, Evans Memorial Department of Medicine, Boston University Medical Center, Boston, Massachusetts

This review focuses on the role of oxidative processes in atherosclerosis and its resultant cardiovascular events. There is now a consensus that atherosclerosis represents a state of heightened oxidative stress characterized by lipid and protein oxidation in the vascular wall. The oxidative modification hypothesis of atherosclerosis predicts that low-density lipoprotein (LDL) oxidation is an early event in atherosclerosis and that oxidized LDL contributes to atherogenesis. In support of this hypothesis, oxidized LDL can support foam cell formation in vitro, the lipid in human lesions is substantially oxidized, there is evidence for the presence of oxidized LDL in vivo, oxidized LDL has a number of potentially proatherogenic activities, and several structurally unrelated antioxidants inhibit atherosclerosis in animals. An emerging consensus also underscores the importance in vascular disease of oxidative events in addition to LDL oxidation. These include the production of reactive oxygen and nitrogen species by vascular cells, as well as oxidative modifications contributing to important clinical manifestations of coronary artery disease such as endothelial dysfunction and plaque disruption. Despite these abundant data however, fundamental problems remain with implicating oxidative modification as a (requisite) pathophysiologically important cause for atherosclerosis. These include the poor performance of antioxidant strategies in limiting either atherosclerosis or cardiovascular events from atherosclerosis, and observations in animals that suggest dissociation between atherosclerosis and lipoprotein oxidation. Indeed, it remains to be established that oxidative events are a cause rather than an injurious response to atherogenesis. In this context, inflammation needs to be considered as a primary process of atherosclerosis, and oxidative stress as a secondary event. To address this issue, we have proposed an "oxidative response to inflammation" model as a means of reconciling the response-to-injury and oxidative modification hypotheses of atherosclerosis.

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				D. G. Yanbaeva, M. A. Dentener, E. C. Creutzberg, G. Wesseling, and E. F. M. Wouters Systemic Effects of Smoking Chest, May 1, 2007; 131(5): 1557 - 1566. [Abstract] [Full Text] [PDF]

				B. J. Wu, N. Di Girolamo, K. Beck, C. G. Hanratty, K. Choy, J. Y. Hou, M. R. Ward, and R. Stocker Probucol [4,4'-[(1-Methylethylidene)bis(thio)]bis-[2,6-bis(1,1-dimethylethyl)phenol]] Inhibits Compensatory Remodeling and Promotes Lumen Loss Associated with Atherosclerosis in Apolipoprotein E-Deficient Mice J. Pharmacol. Exp. Ther., May 1, 2007; 321(2): 477 - 484. [Abstract] [Full Text] [PDF]

				S. Horke, I. Witte, P. Wilgenbus, M. Kruger, D. Strand, and U. Forstermann Paraoxonase-2 Reduces Oxidative Stress in Vascular Cells and Decreases Endoplasmic Reticulum Stress-Induced Caspase Activation Circulation, April 17, 2007; 115(15): 2055 - 2064. [Abstract] [Full Text] [PDF]

				M. Torzewski, V. Ochsenhirt, A. L. Kleschyov, M. Oelze, A. Daiber, H. Li, H. Rossmann, S. Tsimikas, K. Reifenberg, F. Cheng, et al. Deficiency of Glutathione Peroxidase-1 Accelerates the Progression of Atherosclerosis in Apolipoprotein E-Deficient Mice Arterioscler Thromb Vasc Biol, April 1, 2007; 27(4): 850 - 857. [Abstract] [Full Text] [PDF]

				R. Li, W. Chen, R. Yanes, S. Lee, and J. A. Berliner OKL38 is an oxidative stress response gene stimulated by oxidized phospholipids J. Lipid Res., March 1, 2007; 48(3): 709 - 715. [Abstract] [Full Text] [PDF]

				E. Dyroy, T. H. Rost, R. J. Pettersen, B. Halvorsen, O. A. Gudbrandsen, T. Ueland, Z. Muna, F. Muller, J. E. Nordrehaug, P. Aukrust, et al. Tetradecylselenoacetic Acid, a PPAR Ligand With Antioxidant, Antiinflammatory, and Hypolipidemic Properties Arterioscler Thromb Vasc Biol, March 1, 2007; 27(3): 628 - 634. [Abstract] [Full Text] [PDF]

				M. L. McCormick, D. Gavrila, and N. L. Weintraub Role of Oxidative Stress in the Pathogenesis of Abdominal Aortic Aneurysms Arterioscler Thromb Vasc Biol, March 1, 2007; 27(3): 461 - 469. [Abstract] [Full Text] [PDF]

				H. Zhang, Y. Luo, W. Zhang, Y. He, S. Dai, R. Zhang, Y. Huang, P. Bernatchez, F. J. Giordano, G. Shadel, et al. Endothelial-Specific Expression of Mitochondrial Thioredoxin Improves Endothelial Cell Function and Reduces Atherosclerotic Lesions Am. J. Pathol., March 1, 2007; 170(3): 1108 - 1120. [Abstract] [Full Text] [PDF]

				A. E. Silver, S. D. Beske, D. D. Christou, A. J. Donato, K. L. Moreau, I. Eskurza, P. E. Gates, and D. R. Seals Overweight and Obese Humans Demonstrate Increased Vascular Endothelial NAD(P)H Oxidase-p47phox Expression and Evidence of Endothelial Oxidative Stress Circulation, February 6, 2007; 115(5): 627 - 637. [Abstract] [Full Text] [PDF]

				J. Li, V. Savransky, A. Nanayakkara, P. L. Smith, C. P. O'Donnell, and V. Y. Polotsky Hyperlipidemia and lipid peroxidation are dependent on the severity of chronic intermittent hypoxia J Appl Physiol, February 1, 2007; 102(2): 557 - 563. [Abstract] [Full Text] [PDF]

				T. Kriska, G. K. Marathe, J. C. Schmidt, T. M. McIntyre, and A. W. Girotti Phospholipase Action of Platelet-activating Factor Acetylhydrolase, but Not Paraoxonase-1, on Long Fatty Acyl Chain Phospholipid Hydroperoxides J. Biol. Chem., January 5, 2007; 282(1): 100 - 108. [Abstract] [Full Text] [PDF]

				K. Bedard and K.-H. Krause The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology Physiol Rev, January 1, 2007; 87(1): 245 - 313. [Abstract] [Full Text] [PDF]

				A. L. Fitzpatrick, R. A. Kronmal, J. P. Gardner, B. M. Psaty, N. S. Jenny, R. P. Tracy, J. Walston, M. Kimura, and A. Aviv Leukocyte Telomere Length and Cardiovascular Disease in the Cardiovascular Health Study Am. J. Epidemiol., January 1, 2007; 165(1): 14 - 21. [Abstract] [Full Text] [PDF]