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- W2912853526 abstract "Reactive oxygen species (ROS) have an equivocal role in myocardial ischaemia reperfusion injury. Within the cardiomyocyte, mitochondria are both a major source and target of ROS. We evaluate the effects of a selective, dose-dependent increase in mitochondrial ROS levels on cardiac physiology using the mitochondria-targeted redox cycler MitoParaquat (MitoPQ). Low levels of ROS decrease the susceptibility of neonatal rat ventricular myocytes (NRVMs) to anoxia/reoxygenation injury and also cause profound protection in an in vivo mouse model of ischaemia/reperfusion. However higher doses of MitoPQ resulted in a progressive alteration of intracellular [Ca2+] homeostasis and mitochondrial function in vitro, leading to dysfunction and death at high doses. Our data show that a primary increase in mitochondrial ROS can alter cellular function, and support a hormetic model in which low levels of ROS are cardioprotective while higher levels of ROS are cardiotoxic." @default.
- W2912853526 created "2019-02-21" @default.
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- W2912853526 date "2019-04-01" @default.
- W2912853526 modified "2023-10-14" @default.
- W2912853526 title "Selective mitochondrial superoxide generation in vivo is cardioprotective through hormesis" @default.
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- W2912853526 doi "https://doi.org/10.1016/j.freeradbiomed.2019.01.034" @default.
- W2912853526 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6607027" @default.
- W2912853526 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30731114" @default.
- W2912853526 hasPublicationYear "2019" @default.
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