The mitochondrial permeability transition pore and its role in myocardial ischemia reperfusion injury.
Explore this paper's citation graph
Summary
The role of the MPTP is reviewed as a mediator of acute myocardial IRI and as a therapeutic target for cardioprotection.
- Type
- review
- Published
- 2015-01-01
- Cited by
- 316
- References
- 171
- Access
- Open access
- OpenAlex
- https://openalex.org/W2067143095
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:205814556
Keywords
MPTP, Mitochondrial permeability transition pore, Cardioprotection, Myocardial infarction, Medicine
References
- Cyclosporin inhibits mitochondrial calcium efflux in isolated adult rat ventricular cardiomyocytes.
- Ischaemic Preconditioning Inhibits Opening of Mitochondrial Permeability Transition Pores in the Reperfused Rat Heart
- Remote ischaemic preconditioning: underlying mechanisms and clinical application.
- Role of sarcoplasmic reticulum in mitochondrial permeability transition and cardiomyocyte death during reperfusion.
- Protective Role of Transient Pore Openings in Calcium Handling by Cardiac Mitochondria*
- Evidence for the presence of a reversible Ca2+-dependent pore activated by oxidative stress in heart mitochondria.
- The mitochondrial permeability transition pore.
- Myocardial Reperfusion Injury
- The Ca2+-induced membrane transition in mitochondria. II. Nature of the Ca2+ trigger site.
- Modulation of the mitochondrial permeability transition pore. Effect of protons and divalent cations.
- Rapid accumulation of Akt in mitochondria following phosphatidylinositol 3‐kinase activation
- The Ca2+-induced membrane transition in mitochondria. III. Transitional Ca2+ release.
- Mitochondrial fusion and fission proteins: novel therapeutic targets for combating cardiovascular disease
- The reversible Ca2+-induced permeabilization of rat liver mitochondria.
- Relationship between configuration, function, and permeability in calcium-treated mitochondria.
- Targeting hexokinase II to mitochondria to modulate energy metabolism and reduce ischaemia‐reperfusion injury in heart
- Cyclosporin A and cardioprotection: from investigative tool to therapeutic agent
- Kinetic evidence for a heart mitochondrial pore activated by Ca2+, inorganic phosphate and oxidative stress. A potential mechanism for mitochondrial dysfunction during cellular Ca2+ overload.
- Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion.
- The Ca2+-induced membrane transition in mitochondria. I. The protective mechanisms.
Cited by
- Coordination of cellular localization-dependent effects of SUMOylation in regulating cardiovascular and neurological diseases
- Cytochrome P450‐derived eicosanoids and heart function
- A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation.
- Reperfusion injury and reactive oxygen species: The evolution of a concept
- Nitrite Confers Preconditioning and Cytoprotection After Ischemia/Reperfusion Injury Through the Modulation of Mitochondrial Function
- Febuxostat pretreatment attenuates myocardial ischemia/reperfusion injury via mitochondrial apoptosis
- Protective role of melatonin in mitochondrial dysfunction and related disorders
- Noninvasive vagus nerve stimulation: A novel feasible approach for cardioprotection during ischemia-reperfusion injury.
- Parkin Gone Wild: Unbridled Ubiquitination
- Catch me if you can: targeting the mitochondrial permeability transition pore in myocardial infarction
- Dexmedetomidine protects the heart against ischemia-reperfusion injury by an endothelial eNOS/NO dependent mechanism.
- Reducing myocardial infarct size: challenges and future opportunities
- Cardiolipin alterations and mitochondrial dysfunction in heart ischemia/reperfusion injury
- Improved heart function from older donors using pharmacologic conditioning strategies.
- RP105-PI3K-Akt axis: A potential therapeutic approach for ameliorating myocardial ischemia/reperfusion injury.
- Chronic heart failure: Ca2+, catabolism, and catastrophic cell death
- Cyclosporine-A mimicked the ischemic pre- and postconditioning-mediated cardioprotection in hypertensive rats: Role of PKCε.
- Quantification of active mitochondrial permeability transition pores using GNX-4975 inhibitor titrations provides insights into molecular identity
- Ischaemic conditioning and reperfusion injury
- The role of the beta3-adrenergic receptor (β3-AR) in cardioprotection
Related papers
- Sanglifehrin A inhibits opening of mitochondrial permeability transition pore (MPTP) during ischemia/reperfusion in the adult but not in the immature heart
- Mitochondrial Permeability Transition Pore-Dependent Necrosis
- Preconditioning and postconditioning
- Inhibition of Bcl-2 Sensitizes Mitochondrial Permeability Transition Pore (MPTP) Opening in Ischemia-Damaged Mitochondria
- PERSISTENT INHIBITION OF MITOCHONDRIAL PERMEABILITY TRANSITION BY PRECONDITIONING DURING THE FIRST HOURS OF REPERFUSION
- Molecular identity of the mitochondrial permeability transition pore and its role in ischemia-reperfusion injury.
- The Mitochondrial Permeability Transition Pore – a Regulator of the Resistance of the Heart to Reperfusion
- Permeability-Controlled Probe for Directly Visualizing the Opening of Mitochondrial Permeability Transition Pore in Native Status.
- The roles of phosphate and the phosphate carrier in the mitochondrial permeability transition pore