title: Hydrogen sulfide and cell signaling.
abstract: Hydrogen sulfide (H₂S) is a gaseous mediator synthesized from cysteine by cystathionine γ lyase (CSE) and other naturally occurring enzymes. Pharmacological experiments using H₂S donors and genetic experiments using CSE knockout mice suggest important roles for this vasodilator gas in the regulation of blood vessel caliber, cardiac response to ischemia/reperfusion injury, and inflammation. That H₂S inhibits cytochrome c oxidase and reduces cell energy production has been known for many decades, but more recently, a number of additional pharmacological targets for this gas have been identified. H₂S activates K(ATP) and transient receptor potential (TRP) channels but usually inhibits big conductance Ca²(+)-sensitive K(+) (BK(Ca)) channels, T-type calcium channels, and M-type calcium channels. H₂S may inhibit or activate NF-κB nuclear translocation while affecting the activity of numerous kinases including p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and Akt. These disparate effects may be secondary to the well-known reducing activity of H₂S and/or its ability to promote sulfhydration of protein cysteine moieties within the cell.
authors.affiliation: Imperial College London, United Kingdom.
authors.forename: Ling
authors.initials: L
authors.lastname: Li
authors.forename: Peter
authors.initials: P
authors.lastname: Rose
authors.forename: Philip K
authors.initials: PK
authors.lastname: Moore
mesh_terms: D000818:Animals; D003542:Cystathionine gamma-Lyase / Q000378:metabolism*; D003545:Cysteine / Q000378:metabolism; D006801:Humans; D006862:Hydrogen Sulfide / Q000378:metabolism*; D051379:Mice; D018345:Mice, Knockout; D015398:Signal Transduction; D014664:Vasodilation
chemical_list: D003542:Cystathionine gamma-Lyase; D003545:Cysteine; D006862:Hydrogen Sulfide