The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
The mitochondrial permeability transition pore and ischemia-reperfusion injury
Open accessAbstract
Mitochondrial dysfunction is an underlying cause of ischemia-reperfusion injury. In particular, ischemic injury induces dramatic increases in mitochondrial permeability, thereby instigating a chain of events that leads to both apoptotic and necrotic cardiomyocyte death. The mitochondrial permeability transition (MPT) pore, a large, non-specific channel that spans the inner mitochondrial membrane, is known to mediate the lethal permeability changes that initiate mitochondrial-driven cardiomyocyte death. The purpose of this review is to focus on the role of the MPT pore in ischemia-reperfusion injury, the mechanisms involved, and, in particular, what we do and do not know regarding the pore’s molecular composition.
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Cites
Mitochondrial membrane permeabilization in cell death
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“Unlike VDAC and ANT, there is only one known gene for CypD (the Ppif gene), and, several groups, including our own, have independently generated Ppif-null mice [5, 7, 52, 63].”
BackgroundResultInfluentialBax and Adenine Nucleotide Translocator Cooperate in the Mitochondrial Control of Apoptosis
Marzo, I., Brenner, C., Zamzami, N., Jürgensmeier, J. M., Susin, S. A., Vieira, H. L. A., Prévost, M.-C., Xie, Z., Matsuyama, S., Reed, J. C., et al. (1998) · Science · doi:10.1126/science.281.5385.2027 · Cited by 1,168
The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore
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Properties of the Permeability Transition Pore in Mitochondria Devoid of Cyclophilin D
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“If the elevations in mitochondrial Ca become excessive they can trigger the MPT response [5, 7, 15, 19, 41, 42].”
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Response to myocardial ischemia/reperfusion injury involves Bnip3 and autophagy
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Cited by
Necroptosis in health and diseases
Zhou, W., & Yuan, J. (2014) · Seminars in Cell & Developmental Biology · doi:10.1016/j.semcdb.2014.07.013 · Cited by 414
Cardioprotective and Antiapoptotic Effects of Heme Oxygenase-1 in the Failing Heart
Wang, G., Hamid, T., Keith, R. J., Zhou, G., Partridge, C. R., Xiang, X., Kingery, J. R., Lewis, R. K., Li, Q., Rokosh, D. G., et al. (2010) · Circulation · doi:10.1161/circulationaha.109.905471 · Cited by 249
Wang, L., Liu, Y., Zhang, X., Ye, Y., Xiong, X., Zhang, S., Gu, L., Jian, Z., & Wang, H. (2022) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.864426 · Cited by 121
Liu, C., Yang, F., Cheng, S., Liu, Y., Wan, L., & Cong, H. (2017) · Cardiovascular Therapeutics · doi:10.1111/1755-5922.12225 · Cited by 52
Cardioprotection and thyroid hormones
Pingitore, A., Nicolini, G., Kusmic, C., Iervasi, G., Grigolini, P., & Forini, F. (2016) · Heart Failure Reviews · doi:10.1007/s10741-016-9545-8 · Cited by 51
Metadata
- Authors
- Baines, C. P.
- Venue
- Basic Research in Cardiology
- Published
- 2009-02-26
- Volume
- 104
- Issue
- 2
- Pages
- 181-188
- ISSN
- 0003-9217 (ISSN-L)
- 0300-8428
- 1435-1803
- OpenAlex
- W2024870847
- Cited by
- 280
- References
- 10
- FWCI
- 14.93
- Type
- journal article
- Language
- en
- Open access
- green
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