Myocardial Ischemic Postconditioning Promotes Autophagy against Ischemia Reperfusion Injury via the Activation of the nNOS/AMPK/mTOR Pathway
| العنوان: | Myocardial Ischemic Postconditioning Promotes Autophagy against Ischemia Reperfusion Injury via the Activation of the nNOS/AMPK/mTOR Pathway |
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| المؤلفون: | Suhua Zhu, Qing-Ping Li, Xiaowei Wu, Hong-Yi Zhu, Liang Hu, Maojuan Hao |
| المصدر: | International Journal of Molecular Sciences International Journal of Molecular Sciences; Volume 18; Issue 3; Pages: 614 International Journal of Molecular Sciences, Vol 18, Iss 3, p 614 (2017) |
| بيانات النشر: | MDPI AG, 2017. |
| سنة النشر: | 2017 |
| مصطلحات موضوعية: | Male, 0301 basic medicine, Nitric Oxide Synthase Type I, AMP-Activated Protein Kinases, lcsh:Chemistry, Mice, Ischemic Postconditioning, lcsh:QH301-705.5, Spectroscopy, chemistry.chemical_classification, TOR Serine-Threonine Kinases, mammalian target of rapamycin (mTOR), General Medicine, Mitochondria, Computer Science Applications, Cell biology, Reperfusion Injury, cardiovascular system, Signal Transduction, medicine.drug, autophagy, adenosine monophosphate-activated protein kinase (AMPK), medicine.medical_specialty, Article, Catalysis, Cell Line, Inorganic Chemistry, 03 medical and health sciences, Internal medicine, medicine, Animals, Physical and Theoretical Chemistry, Protein kinase A, ischemic postconditioning (IPostC), ischemia/reperfusion, neuronal nitric oxide synthase (nNOS), Molecular Biology, PI3K/AKT/mTOR pathway, Reactive oxygen species, Myocardium, Organic Chemistry, Autophagy, AMPK, medicine.disease, Adenosine, 030104 developmental biology, Endocrinology, lcsh:Biology (General), lcsh:QD1-999, chemistry, Apoptosis, Reperfusion injury |
| الوصف: | 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. |
| وصف الملف: | application/pdf |
| تدمد: | 1422-0067 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b699fa81934a03619a9805f733e92b6dTest https://doi.org/10.3390/ijms18030614Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....b699fa81934a03619a9805f733e92b6d |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14220067 |
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