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- W2051551158 endingPage "706" @default.
- W2051551158 startingPage "700" @default.
- W2051551158 abstract "The molecular events occurring during myocardial infarction and cardioprotection are described with an emphasis on the changes of the mitochondrial membrane potential (ΔΨm). The low ΔΨm values of the normal beating heart (100–140 mV) are explained by the allosteric ATP-inhibition of cytochrome c oxidase (CcO) through feedback inhibition by ATP at high [ATP]/[ADP] ratios. During ischemia the mechanism is reversibly switched off by signaling through reactive oxygen species (ROS). At reperfusion high ΔΨm values cause a burst of ROS production leading to apoptosis and/or necrosis. Ischemic preconditioning is suggested to cause additional phosphorylation of CcO, protecting the enzyme from immediate dephosphorylation via ROS signaling." @default.
- W2051551158 created "2016-06-24" @default.
- W2051551158 creator A5012624684 @default.
- W2051551158 creator A5016664198 @default.
- W2051551158 creator A5063779503 @default.
- W2051551158 creator A5080427205 @default.
- W2051551158 date "2011-09-01" @default.
- W2051551158 modified "2023-09-24" @default.
- W2051551158 title "The role of mitochondrial membrane potential in ischemic heart failure" @default.
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