Hydrogen Sulfide and Cell Signalingreview
Аннотация: 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.
Год издания: 2011
Авторы: Ling Li, Peter Rose, Philip K. Moore
Издательство: Annual Reviews
Источник: The Annual Review of Pharmacology and Toxicology
Ключевые слова: Sulfur Compounds in Biology, Eicosanoids and Hypertension Pharmacology, Nitric Oxide and Endothelin Effects
Другие ссылки: The Annual Review of Pharmacology and Toxicology (HTML)
PubMed (HTML)
PubMed (HTML)
Открытый доступ: closed
Том: 51
Выпуск: 1
Страницы: 169–187