Hydrogen sulfide and cell signaling

Li, Ling and Rose, Peter and Moore, Philip K. (2011) Hydrogen sulfide and cell signaling. Annual Review of Pharmacology and Toxicology, 51 (1). pp. 169-187. ISSN 0362-1642

Full content URL: http://dx.doi.org/10.1146/annurev-pharmtox-010510-...

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Item Type:Article
Item Status:Live Archive

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.

Keywords:Cell signalling, Hydrogen sulfide, Hydrogen sulphide
Subjects:B Subjects allied to Medicine > B100 Anatomy, Physiology and Pathology
Divisions:College of Science > School of Life Sciences
ID Code:9806
Deposited On:10 Jun 2013 11:40

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