Mitochondrial permeability transition pore opening during myocardial reperfusion--a target for cardioprotection.
By A. Halestrap, S. Clarke, S. Javadov. Cardiovascular Research, 2004
1,261 citations recorded by the source corpus.
Subfields: Developmental Neuroscience, Emergency Medicine, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/8d50ed8445adf4abc70d74e0aa6c501190e82bb1
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In Developmental Neuroscience
In Emergency Medicine
In Pathology and Forensic Medicine
Citations in the corpus
- Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning (2007, background): “(Crompton, 1999; Hajnóczky et al., 2000; Bishopric et al., 2001; Di Lisa et al., 2001; Pacher and Hajnóczky, 2001; Pacher et al., 2001; Halestrap et al., 2004).”
- Mitochondrial function as a therapeutic target in heart failure (2016, neutral): “Increased proclivity of MPTP opening occurs in both acute and chronic heart disease, and numerous preclinical studies have demonstrated efficacy in cardiac pathology with MPTP blockers, such as cyclosporin, NIM811, and TRO40303 (reviewed previously 175–179 ).”
- Reactive Oxygen Species in Inflammation and Tissue Injury (2014, positive): “Independent of apoptosis by Bcl-2 family members, the mitochondrial permeability transition (MPT) induced by the opening of mitochondrial permeability transition pore (mPTP) can also lead to cell death.”
- Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “There are considerable data suggesting that inhibitors of MPT, a large conductance channel, reduce ischemia-reperfusion injury (86, 92, 117, 224).”