Sulfane Sustains Vascular Health

Hydrogen sulfide (H2S) is widely known as a pungent toxic gaseous that has plagued humanity in various environmental conditions for centuries. However, H2S, along with nitric oxide (NO) and carbon monoxide (CO), is now recognized to be an important biological gasotransmitter that was previously believed to simply be an environmental toxin.1 H2S can be produced in the mammalian body by 3 enzymes: cystathionine γ-lyase (CSE), cystathionine β synthase, and 3-mercaptopyruvate sulfurtransferase from the substrates cystathionine, homocysteine, cysteine, and mercaptopyruvate. Recently, the physiological importance of H2S in the cardiovascular system, particularly vascular growth and inflammatory regulation, has been recognized; however, information on the importance of endogenous H2S synthesis pathways and identification of critical enzymes has been less clear.2 In this issue of Circulation , 2 complementary articles examining endogenous H2S production and metabolism functions provide important insight into the role of CSE and H2S bioavailability for vascular pathophysiological responses during preeclampsia and atherosclerosis. The first article by Wang et al3 emphasizes the emergence of an important role for H2S in regulating placental vasculature dysfunction during preeclampsia by altering placental growth factor, soluble Flt-1 (sFlt-1), and soluble endoglin (sEng) levels. The second article by Mani4 and colleagues provides important insight into the role of endogenous H2S production in modulating atherosclerosis, intimal proliferation, adhesion molecule expression (eg, intercellular adhesion molecule-1), oxidative stress, and lipid metabolism.Articles see p 2514 and p 2523Preeclampsia is a pregnancy-related vascular disorder characterized by hypertension, proteinuria, and peripheral edema. Although the exact cause of preeclampsia is unknown, possible causes include systemic endothelial dysfunction and impaired vascular growth and remodeling in the placenta.5 Human placenta expresses vascular endothelial growth factor and its receptor (flt-1). According …