title: Oxidation-sensitive mechanisms, vascular apoptosis and atherosclerosis.
abstract: Increased generation of oxidants, resulting from disruption of aerobic metabolism and from respiratory burst, is an essential defense mechanism against pathogens and aberrant cells. However, oxidative stress can also trigger and enhance deregulated apoptosis or programmed cell death, characteristic of atherosclerotic lesions. Oxidation-sensitive mechanisms also modulate cellular signaling pathways that regulate vascular expression of cytokines and growth factors, and influence atherogenesis, in particular when increased levels of plasma lipoproteins provide ample substrate for lipid peroxidation and lead to increased formation of adducts with lipoprotein amino acids. In some cases, increased oxidation and apoptosis in a group of cells might be beneficial for survival and function of other groups of arterial cells. However, overall, oxidation and apoptosis appear to promote the progression of diseased arteries towards a lesion that is vulnerable to rupture, and to give rise to myocardial infarction and ischemic stroke. Recent rapid advances in our understanding of the interactions between oxidative stress, apoptosis and arterial gene regulation suggest that selective interventions targeting these biological functions have great therapeutic potential.
authors.affiliation: Department of Pharmacological Sciences, University of Salerno, 84084 Salerno, Italy.
authors.forename: Filomena
authors.initials: F
authors.lastname: de Nigris
authors.forename: Amir
authors.initials: A
authors.lastname: Lerman
authors.forename: Louis J
authors.initials: LJ
authors.lastname: Ignarro
authors.forename: Sharon
authors.initials: S
authors.lastname: Williams-Ignarro
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Sica
authors.forename: Andrew H
authors.initials: AH
authors.lastname: Baker
authors.forename: Lilach O
authors.initials: LO
authors.lastname: Lerman
authors.forename: Yong J
authors.initials: YJ
authors.lastname: Geng
authors.forename: Claudio
authors.initials: C
authors.lastname: Napoli
mesh_terms: D017209:Apoptosis / Q000502:physiology*; D001158:Arteries / Q000378:metabolism / Q000503:physiopathology; D001161:Arteriosclerosis / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D016207:Cytokines / Q000378:metabolism; D005786:Gene Expression Regulation / Q000502:physiology; D015316:Genetic Therapy / Q000379:methods*; D006133:Growth Substances / Q000378:metabolism; D006801:Humans; D008074:Lipoproteins / Q000378:metabolism; D016877:Oxidants / Q000096:biosynthesis; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D016207:Cytokines; D006133:Growth Substances; D008074:Lipoproteins; D016877:Oxidants