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10.15252/embj.201591857 http://scihub22266oqcxt.onion/10.15252/embj.201591857 C4772851!4772851!26843485     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+J 2016 ; 35 (5): 536-52 Nephropedia Template TP {{tp|p=26843485|t=2016. p38? and p38? reprogram liver metabolism by modulating neutrophil infiltration |pdf=|usr=}}{{26843485}} gab.com Text p38 and p38 reprogram liver metabolism by modulating neutrophil infiltration JO: EMBO J http://www.kidney.de/pget.php?&tw=1&pmid=26843485 #FOAvip Non?alcoholic fatty liver disease (NAFLD) is a major health problem and the main cause of liver disease in Western countries. Although NAFLD is strongly associated with obesity and insulin resistance, its pathogenesis remains poorly understood. The disease begins with an excessive accumulation of triglycerides in the liver, which stimulates an inflammatory response. Alternative p38 mitogen?activated kinases (p38? and p38?) have been shown to contribute to inflammation in different diseases. Here we demonstrate that p38? is elevated in livers of obese patients with NAFLD and that mice lacking p38?/? in myeloid cells are resistant to diet?induced fatty liver, hepatic triglyceride accumulation and glucose intolerance. This protective effect is due to defective migration of p38?/??deficient neutrophils to the damaged liver. We further show that neutrophil infiltration in wild?type mice contributes to steatosis development by means of inflammation and liver metabolic changes. Therefore, p38? and p38? in myeloid cells provide a potential target for NAFLD therapy. Twit Text FOAVip p38 and p38 reprogram liver metabolism by modulating neutrophil infiltration ????EMBO J http://www.kidney.de/pget.php?&tw=1&pmid=26843485 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26843485 #FOAvip English Wikipedia <ref>{{Cite pmid|26843485}}</ref> p38? and p38? reprogram liver metabolism by modulating neutrophil infiltration #MMPMID26843485 González?Terán B; Matesanz N; Nikolic I; Verdugo MA; Sreeramkumar V; Hernández?Cosido L; Mora A; Crainiciuc G; Sáiz ML; Bernardo E; Leiva?Vega L; Rodríguez E; Bondía V; Torres JL; Perez?Sieira S; Ortega L; Cuenda A; Sanchez?Madrid F; Nogueiras R; Hidalgo A; Marcos M; Sabio G EMBO J 2016[Mar]; 35 (5): 536-52 PMID26843485show ga Non?alcoholic fatty liver disease (NAFLD) is a major health problem and the main cause of liver disease in Western countries. Although NAFLD is strongly associated with obesity and insulin resistance, its pathogenesis remains poorly understood. The disease begins with an excessive accumulation of triglycerides in the liver, which stimulates an inflammatory response. Alternative p38 mitogen?activated kinases (p38? and p38?) have been shown to contribute to inflammation in different diseases. Here we demonstrate that p38? is elevated in livers of obese patients with NAFLD and that mice lacking p38?/? in myeloid cells are resistant to diet?induced fatty liver, hepatic triglyceride accumulation and glucose intolerance. This protective effect is due to defective migration of p38?/??deficient neutrophils to the damaged liver. We further show that neutrophil infiltration in wild?type mice contributes to steatosis development by means of inflammation and liver metabolic changes. Therefore, p38? and p38? in myeloid cells provide a potential target for NAFLD therapy. äp38? and p38? reprogram liver metabolism by modulating neutrophil infi(epmc).pdf DeepDyve Pubget Overpricing