Inhibition of myocardial reperfusion injury by ischemic postconditioning requires sirtuin 3-mediated deacetylation of cyclophilin D

2015/04/11 by T. Bochaton, Thomas Bochaton, C. Crola-Da-Silva +16 · 26 citations
Medicine · Biochemistry, Genetics and Molecular Biology · #Sirtuins and Resveratrol in Medicine #Cardiac Ischemia and Reperfusion #Signaling Pathways in Disease

paper · doi:10.1016/j.yjmcc.2015.03.017

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• Crosstalk Between Mitochondrial Hyperacetylation and Oxidative Stress in Vascular Dysfunction and Hypertension. [europepmc]
• Novel Molecular Targets Participating in Myocardial Ischemia-Reperfusion Injury and Cardioprotection. [europepmc]
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• Cysteine 202 of cyclophilin D is a site of multiple post-translational modifications and plays a role in cardioprotection. [europepmc]
• Cardiac metabolism as a driver and therapeutic target of myocardial infarction. [europepmc]
• Cyclophilin D: An Integrator of Mitochondrial Function. [europepmc]
• Phosphorylation of cyclophilin D at serine 191 regulates mitochondrial permeability transition pore opening and cell death after ischemia-reperfusion. [europepmc]
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• Sirtuins at the Service of Healthy Longevity. [europepmc]
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• Mitochondrial CypD Acetylation Promotes Endothelial Dysfunction and Hypertension. [europepmc]