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10.1172/JCI87532 http://scihub22266oqcxt.onion/10.1172/JCI87532 C5199713!5199713!27869651     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest ä ; 127 (1): 321-34 Nephropedia Template TP {{tp|p=27869651|t=ä. Pericyte MyD88 and IRAK4 control inflammatory and fibrotic responses to tissue injury |pdf=|usr=}}{{27869651}} gab.com Text Pericyte MyD88 and IRAK4 control inflammatory and fibrotic responses to tissue injury JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=27869651 #FOAvip Fibrotic disease is associated with matrix deposition that results in the loss of organ function. Pericytes, the precursors of myofibroblasts, are a source of pathological matrix collagens and may be promising targets for treating fibrogenesis. Here, we have shown that pericytes activate a TLR2/4- and MyD88-dependent proinflammatory program in response to tissue injury. Similarly to classic immune cells, pericytes activate the NLRP3 inflammasome, leading to IL-1? and IL-18 secretion. Released IL-1? signals through pericyte MyD88 to amplify this response. Unexpectedly, we found that MyD88 and its downstream effector kinase IRAK4 intrinsically control pericyte migration and conversion to myofibroblasts. Specific ablation of MyD88 in pericytes or pharmacological inhibition of MyD88 signaling by an IRAK4 inhibitor in vivo protected against kidney injury by profoundly attenuating tissue injury, activation, and differentiation of myofibroblasts. Our data show that in pericytes, MyD88 and IRAK4 are key regulators of 2 major injury responses: inflammatory and fibrogenic. Moreover, these findings suggest that disruption of this MyD88-dependent pathway in pericytes might be a potential therapeutic approach to inhibit fibrogenesis and promote regeneration. Twit Text FOAVip Pericyte MyD88 and IRAK4 control inflammatory and fibrotic responses to tissue injury ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=27869651 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27869651 #FOAvip English Wikipedia <ref>{{Cite pmid|27869651}}</ref> Pericyte MyD88 and IRAK4 control inflammatory and fibrotic responses to tissue injury #MMPMID27869651 Leaf IA; Nakagawa S; Johnson BG; Cha JJ; Mittelsteadt K; Guckian KM; Gomez IG; Altemeier WA; Duffield JS J Clin Invest ä[]; 127 (1): 321-34 PMID27869651show ga Fibrotic disease is associated with matrix deposition that results in the loss of organ function. Pericytes, the precursors of myofibroblasts, are a source of pathological matrix collagens and may be promising targets for treating fibrogenesis. Here, we have shown that pericytes activate a TLR2/4- and MyD88-dependent proinflammatory program in response to tissue injury. Similarly to classic immune cells, pericytes activate the NLRP3 inflammasome, leading to IL-1? and IL-18 secretion. Released IL-1? signals through pericyte MyD88 to amplify this response. Unexpectedly, we found that MyD88 and its downstream effector kinase IRAK4 intrinsically control pericyte migration and conversion to myofibroblasts. Specific ablation of MyD88 in pericytes or pharmacological inhibition of MyD88 signaling by an IRAK4 inhibitor in vivo protected against kidney injury by profoundly attenuating tissue injury, activation, and differentiation of myofibroblasts. Our data show that in pericytes, MyD88 and IRAK4 are key regulators of 2 major injury responses: inflammatory and fibrogenic. Moreover, these findings suggest that disruption of this MyD88-dependent pathway in pericytes might be a potential therapeutic approach to inhibit fibrogenesis and promote regeneration. äPericyte MyD88 and IRAK4 control inflammatory and fibrotic responses t(epmc).pdf DeepDyve Pubget Overpricing