The DOI matches its Crossref record; 165 of the 165 references it cites were found in a registry or an index.
Cell Death in the Pathogenesis of Heart Disease: Mechanisms and Significance
Open accessAbstract
Cell death was once viewed as unregulated. It is now clear that at least a portion of cell death is a regulated cell suicide process. This type of death can exhibit multiple morphologies. One of these, apoptosis, has long been recognized to be actively mediated, and many of its underlying mechanisms have been elucidated. Moreover, necrosis, the traditional example of unregulated cell death, is also regulated in some instances. Autophagy is usually a survival mechanism but can occur in association with cell death. Little is known, however, about how autophagic cells die. Apoptosis, necrosis, and autophagy occur in cardiac myocytes during myocardial infarction, ischemia/reperfusion, and heart failure. Pharmacological and genetic inhibition of apoptosis and necrosis lessens infarct size and improves cardiac function in these disorders. The roles of autophagy in ischemia/reperfusion and heart failure are unresolved. A better understanding of these processes and their interrelationships may allow for the development of novel therapies for the major heart syndromes.
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
1 retracted
Proapoptotic BAX and BAK Modulate the Unfolded Protein Response by a Direct Interaction with IRE1α
Hetz, C., Bernasconi, P., Fisher, J., Lee, A.-H., Bassik, M. C., Antonsson, B., Brandt, G. S., Iwakoshi, N. N., Schinzel, A., Glimcher, L. H., et al. (2006) · Science · doi:10.1126/science.1123480 · Cited by 667
RetractedLi, P., Nijhawan, D., Budihardjo, I., Srinivasula, S. M., Ahmad, M., Alnemri, E. S., & Wang, X. (1997) · Cell · doi:10.1016/s0092-8674(00)80434-1 · Cited by 7,289
Autophagy in the Pathogenesis of Disease
Levine, B., & Kroemer, G. (2008) · Cell · doi:10.1016/j.cell.2007.12.018 · Cited by 7,069
The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis
Kluck, R. M., Bossy-Wetzel, E., Green, D. R., & Newmeyer, D. D. (1997) · Science · doi:10.1126/science.275.5303.1132 · Cited by 4,714
The BCL-2 protein family: opposing activities that mediate cell death
Youle, R. J., & Strasser, A. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2308 · Cited by 4,679
Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis
Li, H., Zhu, H., Xu, C.-J., & Yuan, J. (1998) · Cell · doi:10.1016/s0092-8674(00)81590-1 · Cited by 4,445
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
Scaffidi, P., Misteli, T., & Bianchi, M. E. (2002) · Nature · doi:10.1038/nature00858 · Cited by 4,221
Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
Wei, M. C., Zong, W.-X., Cheng, E. H.-Y., Lindsten, T., Panoutsakopoulou, V., Ross, A. J., Roth, K. A., MacGregor, G. R., Thompson, C. B., & Korsmeyer, S. J. (2001) · Science · doi:10.1126/science.1059108 · Cited by 3,988
Yellon, D. M., & Hausenloy, D. J. (2007) · New England Journal of Medicine · doi:10.1056/nejmra071667 · Cited by 3,797
Regulation mechanisms and signaling pathways of autophagy
He, C., & Klionsky, D. J. (2009) · Annual Review of Genetics · doi:10.1146/annurev-genet-102808-114910 · Cited by 3,609
Cited by
CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress–induced myocardial necroptosis
Zhang, T., Zhang, Y., Cui, M., Jin, L., Wang, Y., Lv, F., Liu, Y., Zheng, W., Shang, H., Zhang, J., et al. (2016) · Nature Medicine · doi:10.1038/nm.4017 · Cited by 790
D’Mello, M. J. J., Ross, S. A., Briel, M., Anand, S. S., Gerstein, H., & Paré, G. (2015) · Circulation: Cardiovascular Genetics · doi:10.1161/circgenetics.113.000485 · Cited by 350
Bax regulates primary necrosis through mitochondrial dynamics
Whelan, R. S., Konstantinidis, K., Wei, A.-C., Chen, Y., Reyna, D. E., Jha, S., Yang, Y., Calvert, J. W., Lindsten, T., Thompson, C. B., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1201608109 · Cited by 290
Self-citationAkat, K. M., Moore-McGriff, D., Morozov, P., Brown, M., Gogakos, T., Correa Da Rosa, J., Mihailovic, A., Sauer, M., Ji, R., Ramarathnam, A., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1401724111 · Cited by 254
Apoptosis and aging: increased resistance to apoptosis enhances the aging process
Salminen, A., Ojala, J., & Kaarniranta, K. (2011) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-010-0597-y · Cited by 158
Metadata
- Authors
- Whelan, R. S., Kaplinskiy, V., & Kitsis, R. N.
- Venue
- Annual Review of Physiology
- Publisher
- Annual Reviews
- Published
- 2010-03-17
- Volume
- 72
- Issue
- 1
- Pages
- 19-44
- ISSN
- 0066-4278 (ISSN-L)
- 1545-1585
- OpenAlex
- W2170015173
- Cited by
- 759
- References
- 165
- FWCI
- 3.07
- 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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Cell Death in the Pathogenesis of Heart Disease: Mechanisms and Significance. https://app.cochat.ai/papers/10.1146/annurev.physiol.010908.163111
- The paper
- Whelan, R. S., Kaplinskiy, V., & Kitsis, R. N. (2010). Cell Death in the Pathogenesis of Heart Disease: Mechanisms and Significance. Annual Review of Physiology. https://doi.org/10.1146/annurev.physiol.010908.163111
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.
