期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 134, 期 -, 页码 678-687出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2019.01.034
关键词
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资金
- MRC Studentship
- Wellcome Trust [110158/Z/15/Z]
- Leducq Transatlantic Network of Excellence
- COST Action EU-CARDIOPROTECTION [CA16225]
- University of Padova
- MRC [MR/P000320/1]
- MRC [MR/P000320/1] Funding Source: UKRI
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.
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