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10.1093/cvr/cvu027 http://scihub22266oqcxt.onion/10.1093/cvr/cvu027 C3958622!3958622!24501329     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cardiovasc+Res 2014 ; 102 (1): 79-87 Nephropedia Template TP {{tp|p=24501329|t=2014. Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning |pdf=|usr=}}{{24501329}} gab.com Text Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning JO: Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=24501329 #FOAvip Aims: Ischaemic preconditioning (IPC) is an adaptive mechanism that renders the myocardium resistant to injury from subsequent hypoxia. Although reactive oxygen species (ROS) contribute to both the early and late phases of IPC, their enzymatic source and associated signalling events have not yet been understood completely. Our objective was to investigate the role of the Nox1 NADPH oxidase in cardioprotection provided by IPC. Methods and results: Wild-type (WT) and Nox1-deficient mice were treated with three cycles of brief coronary occlusion and reperfusion, followed by prolonged occlusion either immediately (early IPC) or after 24 h (late IPC). Nox1 deficiency had no impact on the cardioprotection afforded by early IPC. In contrast, deficiency of Nox1 during late IPC resulted in a larger infarct size, cardiac remodelling, and increased myocardial apoptosis compared with WT hearts. Furthermore, expression of Nox1 in WT hearts increased in response to late IPC. Deficiency of Nox1 abrogated late IPC-mediated activation of cardiac nuclear factor-?B (NF-?B) and induction of tumour necrosis factor-? (TNF-?) in the heart and circulation. Finally, knockdown of Nox1 in cultured cardiomyocytes prevented TNF-? induction of NF-?B and the protective effect of IPC on hypoxia-induced apoptosis. Conclusions: Our data identify a critical role for Nox1 in late IPC and define a previously unrecognized link between TNF-? and NF-?B in mediating tolerance to myocardial injury. These findings have clinical significance considering the emergence of Nox1 inhibitors for the treatment of cardiovascular disease. Twit Text FOAVip Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning ????Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=24501329 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24501329 #FOAvip English Wikipedia <ref>{{Cite pmid|24501329}}</ref> Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning #MMPMID24501329 Jiang S; Streeter J; Schickling BM; Zimmerman K; Weiss RM; Miller FJ Cardiovasc Res 2014[Apr]; 102 (1): 79-87 PMID24501329show ga Aims: Ischaemic preconditioning (IPC) is an adaptive mechanism that renders the myocardium resistant to injury from subsequent hypoxia. Although reactive oxygen species (ROS) contribute to both the early and late phases of IPC, their enzymatic source and associated signalling events have not yet been understood completely. Our objective was to investigate the role of the Nox1 NADPH oxidase in cardioprotection provided by IPC. Methods and results: Wild-type (WT) and Nox1-deficient mice were treated with three cycles of brief coronary occlusion and reperfusion, followed by prolonged occlusion either immediately (early IPC) or after 24 h (late IPC). Nox1 deficiency had no impact on the cardioprotection afforded by early IPC. In contrast, deficiency of Nox1 during late IPC resulted in a larger infarct size, cardiac remodelling, and increased myocardial apoptosis compared with WT hearts. Furthermore, expression of Nox1 in WT hearts increased in response to late IPC. Deficiency of Nox1 abrogated late IPC-mediated activation of cardiac nuclear factor-?B (NF-?B) and induction of tumour necrosis factor-? (TNF-?) in the heart and circulation. Finally, knockdown of Nox1 in cultured cardiomyocytes prevented TNF-? induction of NF-?B and the protective effect of IPC on hypoxia-induced apoptosis. Conclusions: Our data identify a critical role for Nox1 in late IPC and define a previously unrecognized link between TNF-? and NF-?B in mediating tolerance to myocardial injury. These findings have clinical significance considering the emergence of Nox1 inhibitors for the treatment of cardiovascular disease. äNox1 NADPH oxidase is necessary for late but not early myocardial isch(epmc).pdf DeepDyve Pubget Overpricing