The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Regulation and pharmacology of the mitochondrial permeability transition pore
Open accessAbstract
The 'mitochondrial permeability transition', characterized by a sudden induced change of the inner mitochondrial membrane permeability for water as well as for small substances (</=1.5 kDa), has been known for three decades. Research interest in the entity responsible for this phenomenon, the 'mitochondrial permeability transition pore' (mPTP), has dramatically increased after demonstration that it plays a key role in the life and death decision in cells. Therefore, a better understanding of this phenomenon and its regulation by environmental stresses, kinase signalling, and pharmacological intervention is vital. The characterization of the molecular identity of the mPTP will allow identification of possible pharmacological targets and assist in drug design for its precise regulation. However, despite extensive research efforts, at this point the pore-forming core component(s) of the mPTP remain unidentified. Pivotal new genetic evidence has shown that components once believed to be core elements of the mPTP (namely mitochondrial adenine nucleotide translocator and cyclophilin D) are instead only mPTP regulators (or in the case of voltage-dependent anion channels, probably entirely dispensable). This review provides an update on the current state of knowledge regarding the regulation of the mPTP.
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Baines, C. P., Kaiser, R. A., Purcell, N. H., Blair, N. S., Osinska, H., Hambleton, M. A., Brunskill, E. W., Sayen, M. R., Gottlieb, R. A., Dorn, G. W., et al. (2005) · Nature · doi:10.1038/nature03434 · Cited by 2,280
Nakagawa, T., Shimizu, S., Watanabe, T., Yamaguchi, O., Otsu, K., Yamagata, H., Inohara, H., Kubo, T., & Tsujimoto, Y. (2005) · Nature · doi:10.1038/nature03317 · Cited by 1,635 · cited 1×
“Two other studies demonstrated that cells missing CyP-D are resistant to oxidative stress and Ca2þ overload,(16) and that although they remain quite sensitive to apoptotic stimuli, they become resistant to necrotic death stimuli.(20) This lead to the overall conclusion that mPTP induction may be important for necrosis…”
Reactive Oxygen Species (Ros-Induced) Ros Release
Zorov, D. B., Filburn, C. R., Klotz, L.-O., Zweier, J. L., & Sollott, S. J. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.192.7.1001 · Cited by 1,412
Self-citationThe 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
Isozymes of mammalian hexokinase: structure, subcellular localization and metabolic function
Wilson, J. E. (2003) · Journal of Experimental Biology · doi:10.1242/jeb.00241 · Cited by 1,085
Preconditioning the myocardium: from cellular physiology to clinical cardiology
YELLON, D. M., & DOWNEY, J. M. (2003) · Physiological Reviews · doi:10.1152/physrev.00009.2003 · Cited by 1,062
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
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Mitochondrial Targeted Cyclophilin D Protects Cells from Cell Death by Peptidyl Prolyl Isomerization
Lin, D.-T., & Lechleiter, J. D. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m112035200 · Cited by 181
Cited by
Mitochondrial Reactive Oxygen Species (ROS) and ROS-Induced ROS Release
Zorov, D. B., Juhaszova, M., & Sollott, S. J. (2014) · Physiological Reviews · doi:10.1152/physrev.00026.2013 · Cited by 5,383
Self-citationROS and redox signaling in myocardial ischemia-reperfusion injury and cardioprotection
Cadenas, S. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.01.024 · Cited by 820
Bernardi, P., Rasola, A., Forte, M., & Lippe, G. (2015) · Physiological Reviews · doi:10.1152/physrev.00001.2015 · Cited by 577
Mechanisms of Altered Ca 2+ Handling in Heart Failure
Luo, M., & Anderson, M. E. (2013) · Circulation Research · doi:10.1161/circresaha.113.301651 · Cited by 357
Wang, N., Feng, Y., Zhu, M., Tsang, C., Man, K., Tong, Y., & Tsao, S. (2010) · Journal of Cellular Biochemistry · doi:10.1002/jcb.22869 · Cited by 289
Metadata
- Authors
- Zorov, D. B., Juhaszova, M., Yaniv, Y., Nuss, H. B., Wang, S., & Sollott, S. J.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-05-15
- Volume
- 83
- Issue
- 2
- Pages
- 213-225
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2114429287
- Cited by
- 245
- References
- 9
- FWCI
- 10.56
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Zorov, D. B., Juhaszova, M., Yaniv, Y., Nuss, H. B., Wang, S., & Sollott, S. J. (2009). Regulation and pharmacology of the mitochondrial permeability transition pore. Cardiovascular Research. https://doi.org/10.1093/cvr/cvp151
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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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