The DOI matches its Crossref record; 99 of the 99 references it cites were found in a registry or an index.
Bcl-2 family members and apoptosis, taken to heart
Abstract
Loss of myocardial cells via apoptosis has been observed in many cardiovascular diseases and has been shown to contribute to the initiation and progression of heart failure. The Bcl-2 family members are important regulators of the mitochondrial pathway of apoptosis. These proteins decide whether the mitochondria should initiate the cell death program and release proapoptotic factors such as cytochrome c. The Bcl-2 proteins consist of anti- and proapoptotic members and play a key role in regulating apoptosis in the myocardium. The antiapoptotic proteins have been demonstrated to protect against various cardiac pathologies, whereas the antiapoptotic proteins have been reported to contribute to heart disease. This review summarizes the current understanding of the role of Bcl-2 proteins in the heart.
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Cites
1 retracted
Ku70 suppresses the apoptotic translocation of Bax to mitochondria
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Cited by
Apoptosis and apoptotic body: disease message and therapeutic target potentials
Xu, X., Lai, Y., & Hua, Z.-C. (2019) · Bioscience Reports · doi:10.1042/bsr20180992 · Cited by 909
Heart mitochondria: gates of life and death
Gustafsson, A. B., & Gottlieb, R. A. (2007) · Cardiovascular Research · doi:10.1093/cvr/cvm005 · Cited by 422
Self-citationBnip3 impairs mitochondrial bioenergetics and stimulates mitochondrial turnover
Rikka, S., Quinsay, M. N., Thomas, R. L., Kubli, D. A., Zhang, X., Murphy, A. N., & Gustafsson, Å. B. (2011) · Cell Death & Differentiation · doi:10.1038/cdd.2010.146 · Cited by 277
Self-citationSzczepanek, K., Chen, Q., Larner, A. C., & Lesnefsky, E. J. (2012) · Mitochondrion · doi:10.1016/j.mito.2011.08.011 · Cited by 117
Metadata
- Authors
- Gustafsson, Å. B., & Gottlieb, R. A.
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2007-01
- Volume
- 292
- Issue
- 1
- Pages
- C45-C51
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- OpenAlex
- W1966012757
- Cited by
- 291
- References
- 99
- FWCI
- 6.88
- Type
- journal article
- Language
- en
- Open access
- closed
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