The TRPA1 Channel in the Cardiovascular System: Promising Features and Challenges
The transient receptor potential ankyrin 1 (TRPA1) channel is a calcium-permeable nonselective cation channel in the plasma membrane that belongs to the transient receptor potential (TRP) channel superfamily. Recent studies have suggested that the TRPA1 channel plays an essential role in the develop...
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Published in | Frontiers in pharmacology Vol. 10; p. 1253 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Frontiers Media S.A
18.10.2019
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Subjects | |
Online Access | Get full text |
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Summary: | The transient receptor potential ankyrin 1 (TRPA1) channel is a calcium-permeable nonselective cation channel in the plasma membrane that belongs to the transient receptor potential (TRP) channel superfamily. Recent studies have suggested that the TRPA1 channel plays an essential role in the development and progression of several cardiovascular conditions, such as atherosclerosis, heart failure, myocardial ischemia–reperfusion injury, myocardial fibrosis, arrhythmia, vasodilation, and hypertension. Activation of the TRPA1 channel has a protective effect against the development of atherosclerosis. Furthermore, TRPA1 channel activation elicits peripheral vasodilation and induces a biphasic blood pressure response. However, loss of channel expression or blockade of its activation suppressed heart failure, myocardial ischemia–reperfusion injury, myocardial fibrosis, and arrhythmia. In this paper, we review recent research progress on the TRPA1 channel and discuss its potential role in the cardiovascular system. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 This article was submitted to Cardiovascular and Smooth Muscle Pharmacology, a section of the journal Frontiers in Pharmacology Edited by: Martin C. Michel, Johannes Gutenberg, University Mainz, Germany Reviewed by: Philip Aaronson, King’s College London, United Kingdom; Jennifer Beth Stott, University of London, United Kingdom These authors have contributed equally to this work |
ISSN: | 1663-9812 1663-9812 |
DOI: | 10.3389/fphar.2019.01253 |