期刊
PHYSIOLOGY
卷 29, 期 5, 页码 343-360出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physiol.00009.2014
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资金
- COBRE Program of the National Center for Research Resources - National Institutes of Health (NIH) [2-P20 RR-016435-06]
- American Heart Association Founders Affiliate
- Pulmonary Hypertension Association [10POST3690006]
- American Heart Association (AHA) Scientist Development Grant [13SDG16470005]
- NIH Pathway to Independence Award [1K99 HL-121484-01A1]
- Hemostasis and Thrombosis Program [PHS T32 HL-007594]
- Totman Medical Research Trust
- Fondation Leducq
- NIH [HL-044455, 1P01 HL-095488, R37 DK-053832, R01 HL-098243, 1R01 HL-121706-01]
Endothelial cells and smooth muscle cells of resistance arteries mediate opposing responses to mechanical forces acting on the vasculature, promoting dilation in response to flow and constriction in response to pressure, respectively. In this review, we explore the role of TRP channels, particularly endothelial TRPV4 and smooth muscle TRPC6 and TRPM4 channels, in vascular mechanosensing circuits, placing their putative mechanosensitivity in context with other proposed upstream and downstream signaling pathways.
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