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 accessAbstract
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Spontaneous Hypercholesterolemia and Arterial Lesions in Mice Lacking Apolipoprotein E
Zhang, S. H., Reddick, R. L., Piedrahita, J. A., & Maeda, N. (1992) · Science · doi:10.1126/science.1411543 · Cited by 2,237
Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system
Mehta, P. K., & Griendling, K. K. (2007) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00287.2006 · Cited by 1,924
Isolation and Characterization of a Novel Endogenous Peptide Ligand for the Human APJ Receptor
Tatemoto, K., Hosoya, M., Habata, Y., Fujii, R., Kakegawa, T., Zou, M.-X., Kawamata, Y., Fukusumi, S., Hinuma, S., Kitada, C., et al. (1998) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1998.9489 · Cited by 1,685
Angiotensin II promotes atherosclerotic lesions and aneurysms in apolipoprotein E–deficient mice
Daugherty, A., Manning, M. W., & Cassis, L. A. (2000) · Journal of Clinical Investigation · doi:10.1172/jci7818 · Cited by 1,368
Quantitative assessment of atherosclerotic lesions in mice
Paigen, B., Morrow, A., Holmes, P. A., Mitchell, D., & Williams, R. A. (1987) · Atherosclerosis · doi:10.1016/0021-9150(87)90202-4 · Cited by 952
Piedrahita, J. A., Zhang, S. H., Hagaman, J. R., Oliver, P. M., & Maeda, N. (1992) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.89.10.4471 · Cited by 944
A Domain in TNF Receptors That Mediates Ligand-Independent Receptor Assembly and Signaling
Chan, F. K.-M., Chun, H. J., Zheng, L., Siegel, R. M., Bui, K. L., & Lenardo, M. J. (2000) · Science · doi:10.1126/science.288.5475.2351 · Cited by 856
Self-citationO'Dowd, B. F., Heiber, M., Chan, A., Heng, H. H. Q., Tsui, L.-C., Kennedy, J. L., Shi, X., Petronis, A., George, S. R., & Nguyen, T. (1993) · Gene · doi:10.1016/0378-1119(93)90495-o · Cited by 851
Characterization of Apelin, the Ligand for the APJ Receptor
Lee, D. K., Cheng, R., Nguyen, T., Fan, T., Kariyawasam, A. P., Liu, Y., Osmond, D. H., George, S. R., & O'Dowd, B. F. (2000) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2000.0740034.x · Cited by 682
Renin-angiotensin system and cardiovascular risk
Schmieder, R. E., Hilgers, K. F., Schlaich, M. P., & Schmidt, B. M. (2007) · The Lancet · doi:10.1016/s0140-6736(07)60242-6 · Cited by 663
Cited by
Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome
Maury, E., & Brichard, S. M. (2010) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2009.07.031 · Cited by 1,026
ACE2: The Major Cell Entry Receptor for SARS-CoV-2
Scialo, F., Daniele, A., Amato, F., Pastore, L., Matera, M. G., Cazzola, M., Castaldo, G., & Bianco, A. (2020) · Lung · doi:10.1007/s00408-020-00408-4 · Cited by 481
The exerkine apelin reverses age-associated sarcopenia
Vinel, C., Lukjanenko, L., Batut, A., Deleruyelle, S., Pradère, J.-P., Le Gonidec, S., Dortignac, A., Geoffre, N., Pereira, O., Karaz, S., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0131-6 · Cited by 398
G-Protein–Coupled Receptors in Heart Disease
Wang, J., Gareri, C., & Rockman, H. A. (2018) · Circulation Research · doi:10.1161/circresaha.118.311403 · Cited by 303
MicroRNA-21 Blocks Abdominal Aortic Aneurysm Development and Nicotine-Augmented Expansion
Maegdefessel, L., Azuma, J., Toh, R., Deng, A., Merk, D. R., Raiesdana, A., Leeper, N. J., Raaz, U., Schoelmerich, A. M., McConnell, M. V., et al. (2012) · Science Translational Medicine · doi:10.1126/scitranslmed.3003441 · Cited by 301
Self-citation
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- 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
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.