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DOI 10.1111/bph.13829

Медицинская библиотека · British journal of pharmacology · 2017

Sulfur-containing gaseous signal molecules, ion channels and cardiovascular diseases.

Yu Wen, Jin Hongfang, Tang Chaoshu, Du Junbao, Zhang Zhiren

СтатьяПоддержка исследования: вне правительства СШАОбзорПеревод в очереди

Аннотация

UNLABELLED: Sulfur-containing gaseous signal molecules including hydrogen sulphide and sulfur dioxide were previously recognized as toxic gases. However, extensive studies have revealed that they can be generated in the cardiovascular system via a sulfur-containing amino acid metabolic pathway, and have an important role in cardiovascular physiology and pathophysiology. Ion channels are pore-forming membrane proteins present in the membrane of all biological cells; their functions include the establishment of a resting membrane potential and the control of action potentials and other electrical signals by conducting ions across the cell membrane. Evidence has now accumulated suggesting that the sulfur-containing gaseous signal molecules are important regulators of ion channels and transporters. The aims of this review are (1) to discuss the recent experimental evidences in the cardiovascular system regarding the regulatory effects of sulfur-containing gaseous signal molecules on a variety of ion channels, including ATP-sensitive potassium, calcium-activated potassium, voltage-gated potassium, L- and T-type calcium, transient receptor potential and chloride and sodium channels, and (2) to understand how the gaseous signal molecules affect ion channels and cardiovascular diseases.

LINKED ARTICLES: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc.

Для цитирования: Yu Wen, Jin Hongfang, Tang Chaoshu, Du Junbao, Zhang Zhiren. Sulfur-containing gaseous signal molecules, ion channels and cardiovascular diseases.. British journal of pharmacology. 2017. DOI: 10.1111/bph.13829.

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