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Cited by 329

The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.

Apelin signaling antagonizes Ang II effects in mouse models of atherosclerosis

Open access
Chun, Hyung J., Ali, Ziad A., Kojima, Yoko, Kundu, Ramendra K., Sheikh, Ahmad Y., Agrawal, Rani, Zheng, Lixin, Leeper, Nicholas J., Pearl, Nathan E., Patterson, Andrew J., Anderson, Joshua P., Tsao, Philip S., Lenardo, Michael J., Ashley, Euan A., Quertermous, Thomas·2008·Journal of Clinical Investigation

Abstract

Apelin and its cognate G protein-coupled receptor APJ constitute a signaling pathway with a positive inotropic effect on cardiac function and a vasodepressor function in the systemic circulation. The apelin-APJ pathway appears to have opposing physiological roles to the renin-angiotensin system. Here we investigated whether the apelin-APJ pathway can directly antagonize vascular disease-related Ang II actions. In ApoE-KO mice, exogenous Ang II induced atherosclerosis and abdominal aortic aneurysm formation; we found that coinfusion of apelin abrogated these effects. Similarly, apelin treatment rescued Ang II-mediated increases in neointimal formation and vascular remodeling in a vein graft model. NO has previously been implicated in the vasodepressor function of apelin; we found that apelin treatment increased NO bioavailability in ApoE-KO mice. Furthermore, infusion of an NO synthase inhibitor blocked the apelin-mediated decrease in atherosclerosis and aneurysm formation. In rat primary aortic smooth muscle cells, apelin inhibited Ang II-mediated transcriptional regulation of multiple targets as measured by reporter assays. In addition, we demonstrated by coimmunoprecipitation and fluorescence resonance energy transfer analysis that the Ang II and apelin receptors interacted physically. Taken together, these findings indicate that apelin signaling can block Ang II actions in vascular disease by increasing NO production and inhibiting Ang II cellular signaling.

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Metadata

Authors
Chun, H. J., Ali, Z. A., Kojima, Y., Kundu, R. K., Sheikh, A. Y., Agrawal, R., Zheng, L., Leeper, N. J., Pearl, N. E., Patterson, A. J., Anderson, J. P., Tsao, P. S., Lenardo, M. J., Ashley, E. A., & Quertermous, T.
Venue
Journal of Clinical Investigation
Published
2008-09-01
Volume
118
Issue
10
Pages
3343-54
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2089394474
Cited by
329
References
53
FWCI
10.55
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Apelin signaling antagonizes Ang II effects in mouse models of atherosclerosis. https://app.cochat.ai/papers/10.1172/jci34871
The paper
Chun, H. J., Ali, Z. A., Kojima, Y., Kundu, R. K., Sheikh, A. Y., Agrawal, R., Zheng, L., Leeper, N. J., Pearl, N. E., Patterson, A. J., Anderson, J. P., Tsao, P. S., Lenardo, M. J., Ashley, E. A., & Quertermous, T. (2008). Apelin signaling antagonizes Ang II effects in mouse models of atherosclerosis. Journal of Clinical Investigation. https://doi.org/10.1172/jci34871

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.