期刊
INFLAMMATION
卷 46, 期 4, 页码 1144-1160出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-023-01808-3
关键词
TRPC6; Inflammation; Fibrosis; Signalling; Ion channels
The TRPC subfamily of mammalian Transient Receptor Potential Canonical channels consists of seven transmembrane proteins that form cation channels in mammalian cell plasma membranes. TRPC channels mediate the influx of Ca2+ and Na+ into cells. Deficiency or increased activity of TRPC6 has been linked to various diseases, including kidney disease, pulmonary disease, and neurological disease. This review summarizes the progress made in investigating the physiological roles of TRPC6 and the development of pharmacological tools to modulate its activity.
The mammalian Transient Receptor Potential Canonical (TRPC) subfamily comprises seven transmembrane proteins (TRPC1-7) forming cation channels in the plasma membrane of mammalian cells. TRPC channels mediate Ca2+ and Na+ influx into the cells. Amongst TRPCs, TRPC6 deficiency or increased activity due to gain-of-function mutations has been associated with a multitude of diseases, such as kidney disease, pulmonary disease, and neurological disease. Indeed, the TRPC6 protein is expressed in various organs and is involved in diverse signalling pathways. The last decade saw a surge in the investigative studies concerning the physiological roles of TRPC6 and describing the development of new pharmacological tools modulating TRPC6 activity. The current review summarizes the progress achieved in those investigations.
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