title: Facing up the ROS labyrinth--Where to go?
abstract: Evidence indicates that oxidative stress refers to a condition where cells are subjected to excessive levels of reactive oxygen species (ROS). Overall vascular function is dependent upon a fine balance between oxidant and antioxidant mechanisms which is required, at least in part, for proper functioning of the endothelium. Considerable experimental and clinical data indicate that the intracellular oxidant milieu is also involved in several redox-sensitive cellular signaling pathways, such as ion transport systems, protein phosphorylation, and gene expression and thus also plays important roles as modulator of vascular cell function, such as cell growth, apoptosis, migration, angiogenesis and cell adhesion. Overproduction of ROS under pathophysiologic conditions is integral in the development of vascular disease. This fact stimulated an intensive search of new pharmacological approaches to improve vascular hemeostasis and, particularly those intended to decrease oxidative stress or augment the antioxidant defense mechanisms.
authors.affiliation: School of Medicine, Health Sciences Faculty, Catholic University of Maule, Talca, Chile. arojasr@ucm.cl.
authors.forename: Armando
authors.initials: A
authors.lastname: Rojas
authors.forename: Hector
authors.initials: H
authors.lastname: Figueroa
authors.forename: Miguel A
authors.initials: MA
authors.lastname: Morales
authors.forename: Lamberto
authors.initials: L
authors.lastname: Re
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects / Q000201:enzymology* / Q000503:physiopathology; D005786:Gene Expression Regulation; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D006984:Hypertrophy; D051793:Hypoxia-Inducible Factor 1 / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000235:genetics / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014664:Vasodilation
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000975:Antioxidants; D015815:Cell Adhesion Molecules; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D051793:Hypoxia-Inducible Factor 1; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D018808:Transcription Factor AP-1; D052250:Nitric Oxide Synthase Type III; D011451:Prostaglandin-Endoperoxide Synthases; D019255:NADPH Oxidases