Inhibition of myocardial reperfusion injury by ischemic postconditioning requires sirtuin 3-mediated deacetylation of cyclophilin D. [electronic resource]
Producer: 20160407Description: 61-9 p. digitalISSN:- 1095-8584
- Acetylation
- Animals
- Cell Death
- Cell Hypoxia
- Peptidyl-Prolyl Isomerase F
- Cyclophilins -- metabolism
- Ischemic Postconditioning
- Male
- Membrane Potential, Mitochondrial -- drug effects
- Mice, Knockout
- Mitochondrial Membrane Transport Proteins
- Mitochondrial Permeability Transition Pore
- Myocardial Reperfusion Injury -- metabolism
- Oxygen -- pharmacology
- Rats
- Sirtuin 3 -- metabolism
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't
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