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10.1177/1074248416636477 http://scihub22266oqcxt.onion/10.1177/1074248416636477 C5010518!5010518 !26940570     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26940570 &cmd=llinks): Failed to open stream: HTTP request failed! 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Nicorandil, a Nitric Oxide Donor and ATP-Sensitive Potassium Channel Opener, Protects Against Dystrophin-Deficient Cardiomyopathy |pdf=|usr=}}{{26940570 }} gab.com Text Nicorandil, a Nitric Oxide Donor and ATP-Sensitive Potassium Channel Opener, Protects Against Dystrophin-Deficient Cardiomyopathy JO: J Cardiovasc Pharmacol Ther http://www.kidney.de/pget.php?&tw=1&pmid=26940570 #FOAvip BACKGROUND: Dystrophin-deficient cardiomyopathy is a growing clinical problem without targeted treatments. We investigated whether nicorandil promotes cardioprotection in human dystrophin-deficient induced pluripotent stem cell (iPSC)-derived cardiomyocytes and the muscular dystrophy mdx mouse heart. METHODS AND RESULTS: Dystrophin-deficient iPSC-derived cardiomyocytes had decreased levels of endothelial nitric oxide synthase and neuronal nitric oxide synthase. The dystrophin-deficient cardiomyocytes had increased cell injury and death after 2 hours of stress and recovery. This was associated with increased levels of reactive oxygen species and dissipation of the mitochondrial membrane potential. Nicorandil pretreatment was able to abolish these stress-induced changes through a mechanism that involved the nitric oxide-cyclic guanosine monophosphate pathway and mitochondrial adenosine triphosphate-sensitive potassium channels. The increased reactive oxygen species levels in the dystrophin-deficient cardiomyocytes were associated with diminished expression of select antioxidant genes and increased activity of xanthine oxidase. Furthermore, nicorandil was found to improve the restoration of cardiac function after ischemia and reperfusion in the isolated mdx mouse heart. CONCLUSION: Nicorandil protects against stress-induced cell death in dystrophin-deficient cardiomyocytes and preserves cardiac function in the mdx mouse heart subjected to ischemia and reperfusion injury. This suggests a potential therapeutic role for nicorandil in dystrophin-deficient cardiomyopathy. Twit Text FOAVip Nicorandil, a Nitric Oxide Donor and ATP-Sensitive Potassium Channel Opener, Protects Against Dystrophin-Deficient Cardiomyopathy ????J Cardiovasc Pharmacol Ther http://www.kidney.de/pget.php?&tw=1&pmid=26940570 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26940570 #FOAvip English Wikipedia <ref>{{Cite pmid|26940570 }}</ref> Nicorandil, a Nitric Oxide Donor and ATP-Sensitive Potassium Channel Opener, Protects Against Dystrophin-Deficient Cardiomyopathy #MMPMID26940570 Afzal MZ ; Reiter M ; Gastonguay C ; McGivern JV ; Guan X ; Ge ZD ; Mack DL ; Childers MK ; Ebert AD ; Strande JL J Cardiovasc Pharmacol Ther 2016[Nov]; 21 (6 ): 549-562 PMID26940570 show ga BACKGROUND: Dystrophin-deficient cardiomyopathy is a growing clinical problem without targeted treatments. We investigated whether nicorandil promotes cardioprotection in human dystrophin-deficient induced pluripotent stem cell (iPSC)-derived cardiomyocytes and the muscular dystrophy mdx mouse heart. METHODS AND RESULTS: Dystrophin-deficient iPSC-derived cardiomyocytes had decreased levels of endothelial nitric oxide synthase and neuronal nitric oxide synthase. The dystrophin-deficient cardiomyocytes had increased cell injury and death after 2 hours of stress and recovery. This was associated with increased levels of reactive oxygen species and dissipation of the mitochondrial membrane potential. Nicorandil pretreatment was able to abolish these stress-induced changes through a mechanism that involved the nitric oxide-cyclic guanosine monophosphate pathway and mitochondrial adenosine triphosphate-sensitive potassium channels. The increased reactive oxygen species levels in the dystrophin-deficient cardiomyocytes were associated with diminished expression of select antioxidant genes and increased activity of xanthine oxidase. Furthermore, nicorandil was found to improve the restoration of cardiac function after ischemia and reperfusion in the isolated mdx mouse heart. CONCLUSION: Nicorandil protects against stress-induced cell death in dystrophin-deficient cardiomyocytes and preserves cardiac function in the mdx mouse heart subjected to ischemia and reperfusion injury. This suggests a potential therapeutic role for nicorandil in dystrophin-deficient cardiomyopathy. |Animals [MESH] |Cardiomyopathies/genetics/metabolism/physiopathology/*prevention & control [MESH] |Cell Line [MESH] |Disease Models, Animal [MESH] |Dose-Response Relationship, Drug [MESH] |Humans [MESH] |Induced Pluripotent Stem Cells/*drug effects/metabolism/pathology [MESH] |KATP Channels/*agonists/metabolism [MESH] |Male [MESH] |Mice, Inbred mdx [MESH] |Mitochondria, Heart/drug effects/metabolism/pathology [MESH] |Muscular Dystrophy, Animal/*drug therapy/genetics/metabolism [MESH] |Myocardial Reperfusion Injury/genetics/metabolism/physiopathology/*prevention & control [MESH] |Myocytes, Cardiac/*drug effects/metabolism/pathology [MESH] |Nicorandil/metabolism/*pharmacology [MESH] |Nitric Oxide Donors/metabolism/*pharmacology [MESH] |Nitric Oxide/*metabolism [MESH] |Oxidative Stress/drug effects [MESH] |Reactive Oxygen Species/metabolism [MESH] |Recovery of Function [MESH] |Signal Transduction/drug effects [MESH] |Ventricular Function, Left/drug effects [MESH]Nicorandil, a Nitric Oxide Donor and ATP-Sensitive Potassium Channel O(epmc).pdf DeepDyve Pubget Overpricing