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10.1371/journal.pone.0195604 http://scihub22266oqcxt.onion/10.1371/journal.pone.0195604 C5895022!5895022 !29641598     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29641598 &cmd=llinks): Failed to open stream: HTTP request failed! 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Fasudil improves endothelial dysfunction in rats exposed to chronic intermittent hypoxia through RhoA/ROCK/NFATc3 pathway |pdf=|usr=}}{{29641598 }} gab.com Text Fasudil improves endothelial dysfunction in rats exposed to chronic intermittent hypoxia through RhoA/ROCK/NFATc3 pathway JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29641598 #FOAvip Endothelial dysfunction is one of the main pathological changes in Obstructive sleep apnoea (OSA). The Rho kinase (ROCK) pathway is associated with endothelial dysfunction. However, the interaction between ROCK and nuclear factor of activated T cells isoform c3 (NFATc3) in the development of this pathological response under chronic intermittent hypoxia (CIH) is unclear. To simulate the OSA model, we established a moderate CIH rat model by administering the fraction of inspired O2 (FiO2) from 21% to 9%, 20 times/h, 8 h/day for 3 weeks. Fasudil (ROCK inhibitor, 8 mg/kg/d, i.p.) was administrated in the rats exposed to CIH for 3 weeks. Our results demonstrated that CIH caused significantly endothelial dysfunction, accompanying with increased ET-1 level, decreased eNOS expression and NO production, which reduced ACh-induced vascular relaxation responses. Moreover, RhoA/ROCK-2/NFATc3 expressions were up-regulated. Fasudil significantly improved CIH induced endothelial dysfunction. Data suggested that the ROCK activation is necessary for endothelial dysfunction during CIH. Twit Text FOAVip Fasudil improves endothelial dysfunction in rats exposed to chronic intermittent hypoxia through RhoA/ROCK/NFATc3 pathway ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29641598 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29641598 #FOAvip English Wikipedia <ref>{{Cite pmid|29641598 }}</ref> Fasudil improves endothelial dysfunction in rats exposed to chronic intermittent hypoxia through RhoA/ROCK/NFATc3 pathway #MMPMID29641598 Li JR ; Zhao YS ; Chang Y ; Yang SC ; Guo YJ ; Ji ES PLoS One 2018[]; 13 (4 ): e0195604 PMID29641598 show ga Endothelial dysfunction is one of the main pathological changes in Obstructive sleep apnoea (OSA). The Rho kinase (ROCK) pathway is associated with endothelial dysfunction. However, the interaction between ROCK and nuclear factor of activated T cells isoform c3 (NFATc3) in the development of this pathological response under chronic intermittent hypoxia (CIH) is unclear. To simulate the OSA model, we established a moderate CIH rat model by administering the fraction of inspired O2 (FiO2) from 21% to 9%, 20 times/h, 8 h/day for 3 weeks. Fasudil (ROCK inhibitor, 8 mg/kg/d, i.p.) was administrated in the rats exposed to CIH for 3 weeks. Our results demonstrated that CIH caused significantly endothelial dysfunction, accompanying with increased ET-1 level, decreased eNOS expression and NO production, which reduced ACh-induced vascular relaxation responses. Moreover, RhoA/ROCK-2/NFATc3 expressions were up-regulated. Fasudil significantly improved CIH induced endothelial dysfunction. Data suggested that the ROCK activation is necessary for endothelial dysfunction during CIH. |1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/*analogs & derivatives/pharmacology [MESH] |Animals [MESH] |Aorta/drug effects/pathology/physiopathology [MESH] |Endothelin-1/blood [MESH] |Endothelium, Vascular/*drug effects/*pathology/physiopathology [MESH] |Hypoxia/blood/*pathology/physiopathology [MESH] |Male [MESH] |NFATC Transcription Factors/*metabolism [MESH] |Nitric Oxide/blood [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Signal Transduction/drug effects [MESH] |Time Factors [MESH] |rho-Associated Kinases/*metabolism [MESH]Fasudil improves endothelial dysfunction in rats exposed to chronic in(epmc).pdf DeepDyve Pubget Overpricing