2016
DOI: 10.1038/cddis.2016.108
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Abstract: As a result of its spatial confinement in cardiomyocytes, neuronal nitric oxide synthase (nNOS) is thought to regulate mitochondrial and sarcoplasmic reticulum (SR) function by maintaining nitroso-redox balance and Ca2+ cycling. Thus, we hypothesize that ischemic postconditioning (IPostC) protects hearts against ischemic/reperfusion (I/R) injury through an nNOS-mediated pathway. Isolated mouse hearts were subjected to I/R injury in a Langendorff apparatus, H9C2 cells and primary neonatal rat cardiomyocytes wer… Show more

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Cited by 37 publications
(23 citation statements)
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References 59 publications
(46 reference statements)
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“…Similar findings were obtained in a rabbit model; in that study, nitrate tolerance abolished the protection afforded by IPreC [28,29]. Together, these results highlight the important role of NO in the intracellular signal transduction mechanism of IPreC and IPostC [30,31].…”
Section: Discussionsupporting
confidence: 75%
“…Similar findings were obtained in a rabbit model; in that study, nitrate tolerance abolished the protection afforded by IPreC [28,29]. Together, these results highlight the important role of NO in the intracellular signal transduction mechanism of IPreC and IPostC [30,31].…”
Section: Discussionsupporting
confidence: 75%
“…Short periods of ischemia applied in early minutes of reperfusion reduced infarct size, endothelial dysfunction, accumulation of neutrophils, ROS generation and activated different signaling pathways for cell survival, including ERK1/2 (extracellular signal regulated protein kinase), PI3K-Akt (phosphatidylinositol 3-kinase) 41 neuronal nitric oxide synthase (nNOS) 49 or preventing prolonged opening MPTP 50 .…”
Section: ■ Discussionmentioning
confidence: 99%
“…During IPC, miR-499 knockdown by antagomiR-499 abrogated the cardioprotective effect of IPC against I/R injury as evidenced by increased CK-MB and LDH levels. Oxidative stress is the major trigger and mechanism of myocardial I/R injury and is caused by increased generation of intracellular reactive oxygen species (ROS) [37]. ROS share a paradox with IPC, in that minor levels of I/R or ROS protect the hearts from I/R injury, whereas more profound I/R or ROS formation induces injury [7].…”
Section: Discussionmentioning
confidence: 99%