Mitochondrial Uncoupling Protein 1 Expressed in the Heart of Transgenic Mice Protects Against Ischemic-Reperfusion Damage
作者： Jacqueline Hoerter , Maria-del-Mar Gonzalez-Barroso , Elodie Couplan , Philippe Mateo , Chantal Gelly
DOI: 10.1161/01.CIR.0000137824.30476.0E
关键词: Contractility 、 Inner mitochondrial membrane 、 Biology 、 Mitochondrion 、 Adenosine triphosphate 、 Cell biology 、 Oxidative stress 、 Biochemistry 、 Respiratory system 、 Thermogenin 、 Ischemia
摘要: Background— Mitochondrial respiration is the main source of energy in aerobic animal cells and adapted to demand by respiratory coupling. Uncoupling proteins (UCPs) perturb coupling inducing a proton leak through mitochondrial inner membrane. Although this could lead deleterious waste, it may prevent production oxygen radicals when rate phosphorylation ADP into ATP low, whereas substrate availability mitochondria high. The latter conditions are encountered during cardiac reperfusion after ischemia highly relevant heart infarction. Methods Results— Heart function 6 transgenic mice expressing high amounts UCP1 littermate controls was compared isolated perfused hearts normoxia, 40-minute global ischemia, on reperfusion. In consumption, contractility (quantified as rate-pressure product), their relationship (energetic yield) were similar transge...
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