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10.1016/j.taap.2016.09.011 http://scihub22266oqcxt.onion/10.1016/j.taap.2016.09.011 C5323078!5323078 !27641628     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27641628 &cmd=llinks): Failed to open stream: HTTP request failed! 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A mouse model of alcoholic liver fibrosis-associated acute kidney injury identifies key molecular pathways |pdf=|usr=}}{{27641628 }} gab.com Text A mouse model of alcoholic liver fibrosis-associated acute kidney injury identifies key molecular pathways JO: Toxicol Appl Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=27641628 #FOAvip Clinical data strongly indicate that acute kidney injury (AKI) is a critical complication in alcoholic hepatitis, an acute-on-chronic form of liver failure in patients with advanced alcoholic fibrosis. Development of targeted therapies for AKI in this setting is hampered by the lack of an animal model. To enable research into molecular drivers and novel therapies for fibrosis- and alcohol-associated AKI, we aimed to combine carbon tetrachloride (CCl(4))-induced fibrosis with chronic intra-gastric alcohol feeding. Male C57BL/6J mice were administered a low dose of CCl(4) (0.2ml/kg 2× week/6weeks) followed by alcohol intragastrically (up to 25g/kg/day for 3weeks) and with continued CCl(4). We observed that combined treatment with CCl(4) and alcohol resulted in severe liver injury, more pronounced than using each treatment alone. Importantly, severe kidney injury was evident only in the combined treatment group. This mouse model reproduced distinct pathological features consistent with AKI in human alcoholic hepatitis. Transcriptomic analysis of kidneys revealed profound effects in the combined treatment group, with enrichment for damage-associated pathways, such as apoptosis, inflammation, immune-response and hypoxia. Interestingly, Havcr1 and Lcn2, biomarkers of AKI, were markedly up-regulated. Overall, this study established a novel mouse model of fibrosis- and alcohol-associated AKI and identified key mechanistic pathways. Twit Text FOAVip A mouse model of alcoholic liver fibrosis-associated acute kidney injury identifies key molecular pathways ????Toxicol Appl Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=27641628 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27641628 #FOAvip English Wikipedia <ref>{{Cite pmid|27641628 }}</ref> A mouse model of alcoholic liver fibrosis-associated acute kidney injury identifies key molecular pathways #MMPMID27641628 Furuya S ; Chappell GA ; Iwata Y ; Uehara T ; Kato Y ; Kono H ; Bataller R ; Rusyn I Toxicol Appl Pharmacol 2016[Nov]; 310 (ä): 129-139 PMID27641628 show ga Clinical data strongly indicate that acute kidney injury (AKI) is a critical complication in alcoholic hepatitis, an acute-on-chronic form of liver failure in patients with advanced alcoholic fibrosis. Development of targeted therapies for AKI in this setting is hampered by the lack of an animal model. To enable research into molecular drivers and novel therapies for fibrosis- and alcohol-associated AKI, we aimed to combine carbon tetrachloride (CCl(4))-induced fibrosis with chronic intra-gastric alcohol feeding. Male C57BL/6J mice were administered a low dose of CCl(4) (0.2ml/kg 2× week/6weeks) followed by alcohol intragastrically (up to 25g/kg/day for 3weeks) and with continued CCl(4). We observed that combined treatment with CCl(4) and alcohol resulted in severe liver injury, more pronounced than using each treatment alone. Importantly, severe kidney injury was evident only in the combined treatment group. This mouse model reproduced distinct pathological features consistent with AKI in human alcoholic hepatitis. Transcriptomic analysis of kidneys revealed profound effects in the combined treatment group, with enrichment for damage-associated pathways, such as apoptosis, inflammation, immune-response and hypoxia. Interestingly, Havcr1 and Lcn2, biomarkers of AKI, were markedly up-regulated. Overall, this study established a novel mouse model of fibrosis- and alcohol-associated AKI and identified key mechanistic pathways. |*Disease Models, Animal [MESH] |Acute Kidney Injury/*complications [MESH] |Animals [MESH] |Ethanol/*toxicity [MESH] |Liver Cirrhosis/*complications [MESH] |Male [MESH] |Mice [MESH]A mouse model of alcoholic liver fibrosis-associated acute kidney inju(epmc).pdf DeepDyve Pubget Overpricing