ArticleExperimental and therapeutic medicine2020
Angiotensin type 1 receptor regulates yes-associated protein in vascular endothelial cells.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Review
- Effect of PLC-β1/CaM signaling pathway mediated by AT1R on the occurrence and development of hepatocellular carcinoma.Cancer cell international · 2021Article
- Mst1/2 Kinases Inhibitor, XMU-MP-1, Attenuates Angiotensin II-Induced Ascending Aortic Expansion in Hypercholesterolemic Mice.Circulation reports · 2021Article
- AT1R Regulates Macrophage Polarization Through YAP and Regulates Aortic Dissection Incidence.Frontiers in physiology · 2021Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aortic dissection (AD) is one of the most lethal cardiovascular diseases. Endothelial cell (EC) dysfunction serves an important role in AD progression. Angiotensin II (Ang II) is a key effector in cardiovascular disease development that acts through binding to angiotensin type 1 receptor (AT1R). Yes-associated protein (YAP) is well-known as a key mediator of cell proliferation and apoptosis. To determine whether AT1R and YAP influence EC proliferation or injury, human aortic endothelial cells were cultured under different culture conditions. Using CCK-8 assay, ELISA, western blotting, immunocytochemistry and siRNA transfection, the present study found that Ang II activity reduced EC proliferation, upregulate YAP phosphorylation and result in EC injury that was associated with elevated levels of multiple proinflammatory chemokines. The inhibition of AT1R function, pharmaceutically or via transfection with an AT1R small interfering RNA, alleviated the effects induced by Ang II. Furthermore, AT1R induced YAP phosphorylation via binding to Ang II, and further promoted the inflammation of ECs, along with inhibiting their proliferation.
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Registered trials
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