The DOI matches its Crossref record; 161 of the 161 references it cites were found in a registry or an index.
The mitochondrial permeability transition pore and its role in myocardial ischemia reperfusion injury
Open accessAbstract
Ischemic heart disease (IHD) remains the leading cause of death and disability worldwide. For patients presenting with an acute myocardial infarction, the most effective treatment for limiting myocardial infarct (MI) size is timely reperfusion. However, in addition to the injury incurred during acute myocardial ischemia, the process of reperfusion can itself induce myocardial injury and cardiomyocyte death, termed 'myocardial reperfusion injury', the combination of which can be referred to as acute ischemia-reperfusion injury (IRI). Crucially, there is currently no effective therapy for preventing this form of injury, and novel cardioprotective therapies are therefore required to protect the heart against acute IRI in order to limit MI size and preserve cardiac function. The opening of the mitochondrial permeability transition pore (MPTP) in the first few minutes of reperfusion is known to be a critical determinant of IRI, contributing up to 50% of the final MI size. Importantly, preventing its opening at this time using MPTP inhibitors, such as cyclosporin-A, has been reported in experimental and clinical studies to reduce MI size and preserve cardiac function. However, more specific and novel MPTP inhibitors are required to translate MPTP inhibition as a cardioprotective strategy into clinical practice. In this article, we review the role of the MPTP as a mediator of acute myocardial IRI and as a therapeutic target for cardioprotection. This article is part of a Special Issue entitled "Mitochondria: From Basic Mitochondrial Biology to Cardiovascular Disease".
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Cites
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Self-citationIschaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS
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“They have shown that ischemia results in the myocardial accumulation of the mitochondrial complex II substrate succinate, which at the onset of reperfusion then provides a substrate load to complex II which via reverse electron transport feeds through to complex I, generating the oxidative stress observed in the first…”
BackgroundMyocardial ischemia-reperfusion injury: a neglected therapeutic target
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“Genetic evidence for this role was published in a collection of studies in 2005 [27–29]whichdemonstrated that cardiac mitochondria deficient in CypD were resistant to MPTP opening and the hearts were protected against acute IRI.”
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Cited by
ROS 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
Ischaemic conditioning and targeting reperfusion injury: a 30 year voyage of discovery
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Self-citationInhibition of mitochondrial permeability transition by deletion of the ANT family and CypD
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Mitochondrial Permeability Uncouples Elevated Autophagy and Lifespan Extension
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“10 Cell 177, 1–16, April 4, 2019 ing of mPTP in the first few minutes of reperfusion is known to be a critical determinant of I/R injury (Ong et al., 2015).”
InfluentialMultifunctional Mitochondrial Epac1 Controls Myocardial Cell Death
Fazal, L., Laudette, M., Paula-Gomes, S., Pons, S., Conte, C., Tortosa, F., Sicard, P., Sainte-Marie, Y., Bisserier, M., Lairez, O., et al. (2017) · Circulation Research · doi:10.1161/circresaha.116.309859 · Cited by 111
Metadata
- Authors
- Ong, S.-B., Samangouei, P., Kalkhoran, S. B., & Hausenloy, D. J.
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 2015-01
- Volume
- 78
- Pages
- 23-34
- ISSN
- 0022-2828 (ISSN-L)
- OpenAlex
- W2067143095
- Cited by
- 323
- References
- 161
- FWCI
- 23.12
- Type
- journal article
- Language
- en
- Open access
- green
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- Ong, S.-B., Samangouei, P., Kalkhoran, S. B., & Hausenloy, D. J. (2015). The mitochondrial permeability transition pore and its role in myocardial ischemia reperfusion injury. Journal of Molecular and Cellular Cardiology. https://doi.org/10.1016/j.yjmcc.2014.11.005
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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.
