title: Endothelial dysfunction in acute and chronic coronary syndromes: evidence for a pathogenetic role of oxidative stress.
abstract: The past two decades have highlighted the pivotal role of the endothelium in preserving vascular homeostasis. Among others, nitric oxide (NO) is currently believed to be the main component responsible for endothelium dependent vasorelaxation and therefore for endothelial function integrity. Reduced NO bioavailability causes the so-called "endothelial dysfunction," which seems to be the common molecular disorder comprising stable atherosclerotic narrowing lesions or acute plaque rupture causing unstable angina or myocardial infarction. Compelling evidence is accumulating, stressing the role of oxidative stress in causing reduced NO bioavailability and subsequently endothelial dysfunction (ED). More recently, the role of endothelial cell (EC) apoptosis as a possible final stage of ED and plaque activation has been suggested. In vitro and in vivo evidence suggests a role of oxidative stress also as a putative mechanism finally leading to plaque denudation and activation through increased EC apoptosis. Thus, oxidative stress, irrespective of atherosclerotic disease stages, seems to represent a key phenomenon in vascular disease progression and possible prevention.
authors.affiliation: Department of Cardiology, University of Ferrara c/o Arcispedale S. Anna, Corso Giovecca 203, 44100 Ferrara, Italy. marco.valgimigli@unife.it
authors.forename: Marco
authors.initials: M
authors.lastname: Valgimigli
authors.forename: Elisa
authors.initials: E
authors.lastname: Merli
authors.forename: Patrizia
authors.initials: P
authors.lastname: Malagutti
authors.forename: Olga
authors.initials: O
authors.lastname: Soukhomovskaia
authors.forename: Giordano
authors.initials: G
authors.lastname: Cicchitelli
authors.forename: Gaetano
authors.initials: G
authors.lastname: Macrì
authors.forename: Roberto
authors.initials: R
authors.lastname: Ferrari
mesh_terms: D000208:Acute Disease; D017209:Apoptosis / Q000502:physiology; D015415:Biomarkers / Q000097:blood; D002839:Chromans / Q000494:pharmacology; D002908:Chronic Disease; D003324:Coronary Artery Disease / Q000378:metabolism / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D011379:Prognosis; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D015415:Biomarkers; D002839:Chromans; D007074:Immunoglobulin G; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; C010643:6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid