Title:Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide
Volume: 21
Issue: 32
Author(s): Zaid Altaany, Francesco Moccia, Luca Munaron, Daniele Mancardi and Rui Wang
Affiliation:
Keywords:
Angiogenesis, Endothelial dysfunction, Endothelium, Gasotransmitters, Hydrogen sulfide, Nitric oxide, Snitrosylation,
S-sulfhydration.
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.
