title: Hydrogen sulfide and endothelial dysfunction: relationship with nitric oxide.
abstract: The endothelium is a cellular monolayer that lines the inner surface of blood vessels and plays a central role in the maintenance of cardiovascular homeostasis by controlling platelet aggregation, vascular tone, blood fluidity and fibrinolysis, adhesion and transmigration of inflammatory cells, and angiogenesis. Endothelial dysfunctions are associated with various cardiovascular diseases, including atherosclerosis, hypertension, myocardial infarction, and cardiovascular complications of diabetes. Numerous studies have established the anti-inflammatory, anti-apoptotic, and anti-oxidant effects of hydrogen sulfide (H2S), the latest member to join the gasotransmitter family along with nitric oxide and carbon monoxide, on vascular endothelium. In addition, H2S may prime endothelial cells (ECs) toward angiogenesis and contribute to wound healing, besides to its well-known ability to relax vascular smooth muscle cells (VSMCs), and thereby reducing blood pressure. Finally, H2S may inhibit VSMC proliferation and platelet aggregation. Consistently, a deficit in H2S homeostasis is involved in the pathogenesis of atherosclerosis and of hyperglycaemic endothelial injury. Therefore, the application of H2S-releasing drugs or using gene therapy to increase endogenous H2S level may help restore endothelial function and antagonize the progression of cardiovascular diseases. The present article reviews recent studies on the role of H2S in endothelial homeostasis, under both physiological and pathological conditions, and its putative therapeutic applications.
authors.forename: Zaid
authors.initials: Z
authors.lastname: Altaany
authors.forename: Francesco
authors.initials: F
authors.lastname: Moccia
authors.forename: Luca
authors.initials: L
authors.lastname: Munaron
authors.forename: Daniele
authors.initials: D
authors.lastname: Mancardi
authors.affiliation: Department of Biology - Cardiovascular and Metabolic Research Unit, Lakehead University, Thunder Bay, Ontario, Canada. daniele.mancardi@unito.it.
authors.forename: Rui
authors.initials: R
authors.lastname: Wang
mesh_terms: D000818:Animals; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism* / Q000503:physiopathology; D006862:Hydrogen Sulfide / Q000378:metabolism*; D020138:Hyperhomocysteinemia / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D009569:Nitric Oxide / Q000502:physiology*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III; D006862:Hydrogen Sulfide