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Int. J. Mol. Sci. 2017, 18(3), 614; doi:10.3390/ijms18030614

Myocardial Ischemic Postconditioning Promotes Autophagy against Ischemia Reperfusion Injury via the Activation of the nNOS/AMPK/mTOR Pathway

Department of Pharmacology, Jiangsu Provincial Key Lab of Cardiovascular Diseases and Molecular Intervention, Nanjing Medical University, Nanjing 211166, China
These authors contributed equally to this work.
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Authors to whom correspondence should be addressed.
Academic Editors: H.W.M. Niessen and Paul A.J. Krijnen
Received: 9 January 2017 / Revised: 27 February 2017 / Accepted: 7 March 2017 / Published: 11 March 2017
(This article belongs to the Special Issue Improvement of Cardiac Function in Heart Failure 2017)
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Abstract

Autophagy participates in the progression of many diseases, comprising ischemia/ reperfusion (I/R). It is reported that it is involved in the protective mechanism of ischemic postconditioning (IPostC). According to research, neuronal nitric oxide synthase (nNOS) is also involved in the condition of I/R and IPostC. However, the relationship between nNOS, autophagy and IPostC has not been previously investigated. We hypothesize that IPostC promotes autophagy activity against I/R injury partially through nNOS-mediated pathways. Mouse hearts were subjected to I/R injury through the ligation of the left anterior descending coronary artery. H9c2 cells were subjected to hypoxia/reoxygenation (H/R) in vitro. IPostC, compared with I/R, restored nNOS activity, increased the formation of autophagosome and restored the impaired autophagic flux, thus autophagic activity was raised markedly. IPostC increased adenosine monophosphate-activated protein kinase (AMPK) phosphorylation and suppressed mammalian target of rapamycin (mTOR), but a selective nNOS inhibitor abolished those effects. Similar effects of IPostC were demonstrated in H9c2 cells in vitro. IPostC decreased infarct size and preserved most of the normal structure. The level of reactive oxygen species (ROS) and cell apoptosis were reduced by IPostC with improved cell viability and mitochondrial membrane potential. However, an autophagy inhibitor suppressed the protective effects. These results suggest that IPostC promoted autophagy against I/R injury at least partially via the activation of nNOS/AMPK/mTOR pathway. View Full-Text
Keywords: ischemic postconditioning (IPostC); ischemia/reperfusion; autophagy; neuronal nitric oxide synthase (nNOS); adenosine monophosphate-activated protein kinase (AMPK); mammalian target of rapamycin (mTOR) ischemic postconditioning (IPostC); ischemia/reperfusion; autophagy; neuronal nitric oxide synthase (nNOS); adenosine monophosphate-activated protein kinase (AMPK); mammalian target of rapamycin (mTOR)
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Hao, M.; Zhu, S.; Hu, L.; Zhu, H.; Wu, X.; Li, Q. Myocardial Ischemic Postconditioning Promotes Autophagy against Ischemia Reperfusion Injury via the Activation of the nNOS/AMPK/mTOR Pathway. Int. J. Mol. Sci. 2017, 18, 614.

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