The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
The molecular composition of the mitochondrial permeability transition pore
Open accessAbstract
Uncontrolled cell death is a fundamental cause of organ disease in humans. However, despite the need for us to delineate the molecular machinery that underlies cardiomyocyte death, our knowledge of these lethal cellular processes is still limited. The discovery that mitochondrial dysfunction, and in particular the mitochondrial permeability transition (MPT) pore, is often a common cause of the cardiac cell mortality that underlies numerous cardiac diseases has been a first crucial step. This purpose of this review is to outline our current understanding of the molecular identity of the MPT pore and the many questions that still need to be answered.
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Cites
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
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Reactive Oxygen Species (Ros-Induced) Ros Release
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The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore
Kokoszka, J. E., Waymire, K. G., Levy, S. E., Sligh, J. E., Cai, J., Jones, D. P., MacGregor, G. R., & Wallace, D. C. (2004) · Nature · doi:10.1038/nature02229 · Cited by 1,086
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VDAC2 Inhibits BAK Activation and Mitochondrial Apoptosis
Cheng, E. H.-Y., Sheiko, T. V., Fisher, J. K., Craigen, W. J., & Korsmeyer, S. J. (2003) · Science · doi:10.1126/science.1083995 · Cited by 852
Properties of the Permeability Transition Pore in Mitochondria Devoid of Cyclophilin D
Basso, E., Fante, L., Fowlkes, J., Petronilli, V., Forte, M. A., & Bernardi, P. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.c500089200 · Cited by 808 · cited 1×
“Interestingly, cyclosporine-A was unable to confer additional protection in the CypD-null mitochondria, thereby confirming that CypD is indeed the molecular target for the anti-MPT actions cyclosporine-A [6,79,80].”
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Cited by
Mitochondrial function as a therapeutic target in heart failure
Brown, D. A., Perry, J. B., Allen, M. E., Sabbah, H. N., Stauffer, B. L., Shaikh, S. R., Cleland, J. G. F., Colucci, W. S., Butler, J., Voors, A. A., et al. (2017) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2016.203 · Cited by 803
Kalogeris, T., Baines, C. P., Krenz, M., & Korthuis, R. J. (2016) · Comprehensive Physiology · doi:10.1002/cphy.c160006 · Cited by 718
Self-citationGiorgio, V., Bisetto, E., Soriano, M. E., Dabbeni-Sala, F., Basso, E., Petronilli, V., Forte, M. A., Bernardi, P., & Lippe, G. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.020115 · Cited by 305
A yeast BH3-only protein mediates the mitochondrial pathway of apoptosis
Büttner, S., Ruli, D., Vögtle, F., Galluzzi, L., Moitzi, B., Eisenberg, T., Kepp, O., Habernig, L., Carmona‐Gutierrez, D., Rockenfeller, P., et al. (2011) · The EMBO Journal · doi:10.1038/emboj.2011.197 · Cited by 133
Exercise is muscle mitochondrial medicine
Oliveira, A. N., Richards, B. J., Slavin, M., & Hood, D. A. (2021) · Exercise and Sport Sciences Reviews · doi:10.1249/jes.0000000000000250 · Cited by 26
Metadata
- Authors
- Baines, C. P.
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 2009-06
- Volume
- 46
- Issue
- 6
- Pages
- 850-857
- ISSN
- 0022-2828 (ISSN-L)
- OpenAlex
- W1974718425
- Cited by
- 164
- References
- 11
- FWCI
- 7.68
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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