title: Endothelial dysfunction and atherosclerosis: focus on novel therapeutic approaches.
abstract: Endothelial dysfunction reflected by reduced nitric oxide (NO) availability is certainly the causative factor or promoting mechanism of atherosclerosis. It is necessary to detect endothelial dysfunction at an early stage using appropriate methods, and to choose a treatment for the recovery of endothelial function. There are nonpharmacological and pharmacological therapies to attain endothelial repair. The latter includes the use of renin-angiotensin system inhibitors, statins, erythropoietin, tetrahydrobiopterin, and antioxidants. The pharmacologic therapies are intended to increase NO synthase activity and NO release, inhibit NO degradation, and enhance the activity of endothelial progenitor cells. This article reviews the current knowledge of the pathophysiological events contributing to endothelial dysfunction as well as several established and novel treatment options to reverse those changes along with the discussion of recent patents.
authors.affiliation: 1st Cardiology Department, Hippokration Hospital, Athens University Medical School, Greece.
authors.forename: Alexandros
authors.initials: A
authors.lastname: Briasoulis
authors.forename: Dimitris
authors.initials: D
authors.lastname: Tousoulis
authors.forename: Emmanuel S
authors.initials: ES
authors.lastname: Androulakis
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Papageorgiou
authors.forename: George
authors.initials: G
authors.lastname: Latsios
authors.forename: Christodoulos
authors.initials: C
authors.lastname: Stefanadis
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism*
chemical_list: D009569:Nitric Oxide