The DOI matches its Crossref record; 94 of the 94 references it cites were found in a registry or an index.
Apoptosis in atherosclerosis: beneficial or detrimental?
Open accessAbstract
Several groups have demonstrated apoptotic cell death in atherosclerotic plaques. The significance of apoptosis in atherosclerosis depends on the stage of the plaque, localization and the cell types involved. Both macrophages and smooth muscle cells undergo apoptosis in atherosclerotic plaques. Apoptosis of macrophages is mainly present in regions showing signs of DNA synthesis/repair. Smooth muscle cell apoptosis is mainly present in less cellular regions and is not associated with DNA synthesis/repair. Even in early stages of atherosclerosis smooth muscle cells become susceptible to undergoing apoptosis since they increase different pro-apoptotic factors. Moreover, recent data indicate that smooth muscle cells may be killed by activated macrophages. The loss of the smooth muscle cells can be detrimental for plaque stability since most of the interstitial collagen fibers, which are important for the tensile strength of the fibrous cap, are produced by SMC. Apoptosis of macrophages could be beneficial for plaque stability if apoptotic bodies are removed. Apoptotic cells that are not scavenged in the plaque activate thrombin which could further induce intraplaque thrombosis. It can be concluded that apoptosis in the primary atherosclerosis is detrimental since it could lead to plaque rupture and thrombosis. Recent data of our group indicate that apoptosis decreases after lipid lowering which could be important in our understanding of the cell biology of plaque stabilization.
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
Apoptosis: A Basic Biological Phenomenon with Wideranging Implications in Tissue Kinetics
Kerr, J. F. R., Wyllie, A. H., & Currie, A. R. (1972) · British Journal of Cancer · doi:10.1038/bjc.1972.33 · Cited by 15,725
Tumor suppressor p53 is a direct transcriptional activator of the human bax gene
Toshiyuki, M., & Reed, J. C. (1995) · Cell · doi:10.1016/0092-8674(95)90412-3 · Cited by 4,063
Galis, Z. S., Sukhova, G. K., Lark, M. W., & Libby, P. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117619 · Cited by 2,539
Oxidative stress as a mediator of apoptosis
Buttke, T. M., & Sandstrom, P. A. (1994) · Immunology Today · doi:10.1016/0167-5699(94)90018-3 · Cited by 2,165
Molecular Bases of the Acute Coronary Syndromes
Libby, P. (1995) · Circulation · doi:10.1161/01.cir.91.11.2844 · Cited by 2,028
DNA Deaminating Ability and Genotoxicity of Nitric Oxide and its Progenitors
Wink, D. A., Kasprzak, K. S., Maragos, C. M., Elespuru, R. K., Misra, M., Dunams, T. M., Cebula, T. A., Koch, W. H., Andrews, A. W., Allen, J. S., et al. (1991) · Science · doi:10.1126/science.1948068 · Cited by 1,234
Extensive Nitration of Protein Tyrosines in Human Atherosclerosis Detected by Immunohistochemistry
Beckmann, J. S., Ye, Y. Z., Anderson, P. G., Chen, J., Accavitti, M. A., Tarpey, M. M., & White, C. R. (1994) · Biological Chemistry Hoppe-Seyler · doi:10.1515/bchm3.1994.375.2.81 · Cited by 1,123
DNA damage and mutation in human cells exposed to nitric oxide in vitro.
Nguyen, T., Brunson, D., Crespi, C. L., Penman, B. W., Wishnok, J. S., & Tannenbaum, S. R. (1992) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.89.7.3030 · Cited by 974
Saunders, J. W. (1966) · Science · doi:10.1126/science.154.3749.604 · Cited by 952
Stability and Instability: Two Faces of Coronary Atherosclerosis: The Paul Dudley White Lecture 1995
Davies, M. J. (1996) · Circulation · doi:10.1161/01.cir.94.8.2013 · Cited by 915
Cited by
Anoikis: an emerging hallmark in health and diseases
Taddei, M., Giannoni, E., Fiaschi, T., & Chiarugi, P. (2012) · The Journal of Pathology · doi:10.1002/path.3000 · Cited by 716
Vascular smooth muscle cell death, autophagy and senescence in atherosclerosis
Grootaert, M. O. J., Moulis, M., Roth, L., Martinet, W., Vindis, C., Bennett, M. R., & De Meyer, G. R. Y. (2018) · Cardiovascular Research · doi:10.1093/cvr/cvy007 · Cited by 606
Phagocytosis of apoptotic cells by macrophages is impaired in atherosclerosis
Schrijvers, D. M., De Meyer, G. R. Y., Kockx, M. M., Herman, A. G., & Martinet, W. (2005) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000166517.18801.a7 · Cited by 509
Anoikis: A necessary death program for anchorage-dependent cells
Chiarugi, P., & Giannoni, E. (2008) · Biochemical Pharmacology · doi:10.1016/j.bcp.2008.07.023 · Cited by 494
Pedruzzi, E., Guichard, C., Ollivier, V., Driss, F., Fay, M., Prunet, C., Marie, J.-C., Pouzet, C., Samadi, M., Elbim, C., et al. (2004) · Molecular and Cellular Biology · doi:10.1128/mcb.24.24.10703-10717.2004 · Cited by 435
Metadata
- Authors
- Kockx, M.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-02
- Volume
- 45
- Issue
- 3
- Pages
- 736-746
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2010835380
- Cited by
- 311
- References
- 94
- FWCI
- 7.43
- 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: Apoptosis in atherosclerosis: beneficial or detrimental? https://app.cochat.ai/papers/10.1016/s0008-6363(99)00235-7
- The paper
- Kockx, M. (2000). Apoptosis in atherosclerosis: beneficial or detrimental? Cardiovascular Research. https://doi.org/10.1016/s0008-6363(99)00235-7
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.