Sulfane Sustains Vascular Health: Insights into Cystathionine γ-Lyase Function
Hydrogen sulfide (H2S) is widely known as a pungent toxic gaseous that has plagued humanity in various environmental conditions for centuries. However, H2S is now recognized, along with nitric oxide (NO) and carbon monoxide (CO), to be an important biological gasotransmitter that were all previously believed to simply be environmental toxicants.1 Hydrogen sulfide can be produced in the mammalian body by three enzymes including cystathionine γ-lyase (CSE), cystathionine β synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST) from 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 regarding the importance of endogenous H2S synthesis pathways and identification of critical enzymes has been less clear.2 In this issue of Circulation, two complementary manuscripts 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 (PIGF), soluble Flt-1 (sFlt-1) and soluble endoglin (sEng) levels. Whereas, 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 (e.g. ICAM-1), oxidative stress, and lipid metabolism.
- Received May 20, 2013.
- Accepted May 21, 2013.