Hydrogen sulfide and cell signaling

Annu Rev Pharmacol Toxicol. 2011;51:169-87. doi: 10.1146/annurev-pharmtox-010510-100505.

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Cystathionine gamma-Lyase / metabolism*
  • Cysteine / metabolism
  • Humans
  • Hydrogen Sulfide / metabolism*
  • Mice
  • Mice, Knockout
  • Signal Transduction*
  • Vasodilation

Substances

  • Cystathionine gamma-Lyase
  • Cysteine
  • Hydrogen Sulfide