The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Inhibition of lipoprotein-associated phospholipase A2 reduces complex coronary atherosclerotic plaque development
Open accessAbstract
Increased lipoprotein-associated phospholipase A2 (Lp-PLA2) activity is associated with increased risk of cardiac events, but it is not known whether Lp-PLA2 is a causative agent. Here we show that selective inhibition of Lp-PLA2 with darapladib reduced development of advanced coronary atherosclerosis in diabetic and hypercholesterolemic swine. Darapladib markedly inhibited plasma and lesion Lp-PLA2 activity and reduced lesion lysophosphatidylcholine content. Analysis of coronary gene expression showed that darapladib exerted a general anti-inflammatory action, substantially reducing the expression of 24 genes associated with macrophage and T lymphocyte functioning. Darapladib treatment resulted in a considerable decrease in plaque area and, notably, a markedly reduced necrotic core area and reduced medial destruction, resulting in fewer lesions with an unstable phenotype. These data show that selective inhibition of Lp-PLA2 inhibits progression to advanced coronary atherosclerotic lesions and confirms a crucial role of vascular inflammation independent from hypercholesterolemia in the development of lesions implicated in the pathogenesis of myocardial infarction and stroke.
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
Atherosclerosis--an inflammatory disease
Ross, R. (1999) · New England Journal of Medicine · doi:10.1056/nejm199901143400207 · Cited by 21,725
Tacke, F., Alvarez, D., Kaplan, T. J., Jakubzick, C., Spanbroek, R., Llodra, J., Garin, A., Liu, J., Mack, M., van Rooijen, N., et al. (2007) · Journal of Clinical Investigation · doi:10.1172/jci28549 · Cited by 1,323
Heart Protection Study Collaborative Group (2011) · The Lancet · doi:10.1016/s0140-6736(11)61125-2 · Cited by 373
Garza, C. A., Montori, V. M., McConnell, J. P., Somers, V. K., Kullo, I. J., & Lopez-Jimenez, F. (2007) · Mayo Clinic Proceedings · doi:10.1016/s0025-6196(11)60992-0 · Cited by 159
Van Eck, M., Herijgers, N., Yates, J., Pearce, N. J., Hoogerbrugge, P. M., Groot, P. H. E., & Van Berkel, T. J. C. (1997) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.17.11.3117 · Cited by 96
Cited by
Atherosclerosis: current pathogenesis and therapeutic options
Weber, C., & Noels, H. (2011) · Nature Medicine · doi:10.1038/nm.2538 · Cited by 2,203
Phospholipase A2 structure/function, mechanism, and signaling
Burke, J. E., & Dennis, E. A. (2009) · Journal of Lipid Research · doi:10.1194/jlr.r800033-jlr200 · Cited by 933
Research Progress on the Relationship between Atherosclerosis and Inflammation
Zhu, Y., Xian, X., Wang, Z., Bi, Y., Chen, Q., Han, X., Tang, D., & Chen, R. (2018) · Biomolecules · doi:10.3390/biom8030080 · Cited by 872
An Updated Review of Lysophosphatidylcholine Metabolism in Human Diseases
Law, S.-H., Chan, M.-L., Marathe, G. K., Parveen, F., Chen, C.-H., & Ke, L.-Y. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20051149 · Cited by 817
Genetics of coronary artery disease: discovery, biology and clinical translation
Khera, A. V., & Kathiresan, S. (2017) · Nature Reviews Genetics · doi:10.1038/nrg.2016.160 · Cited by 659
Metadata
- Authors
- Wilensky, R. L., Shi, Y., Mohler, E. R., Hamamdzic, D., Burgert, M. E., Li, J., Postle, A., Fenning, R. S., Bollinger, J. G., Hoffman, B. E., Pelchovitz, D. J., Yang, J., Mirabile, R. C., Webb, C. L., Zhang, L., Zhang, P., Gelb, M. H., Walker, M. C., Zalewski, A., & Macphee, C. H.
- Venue
- Nature Medicine
- Published
- 2008-09-21
- Volume
- 14
- Issue
- 10
- Pages
- 1059-1066
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2099917925
- Cited by
- 387
- References
- 5
- FWCI
- 13.32
- Type
- journal article
- Language
- en
- Open access
- green
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
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.
