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10.1111/apha.12798 http://scihub22266oqcxt.onion/10.1111/apha.12798 C5324638!5324638!27602552     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Acta+Physiol+(Oxf) 2017 ; 219 (3): 573-88 Nephropedia Template TP {{tp|p=27602552|t=2017. Physiological aspects of Toll?like receptor 4 activation in sepsis?induced acute kidney injury |pdf=|usr=}}{{27602552}} gab.com Text Physiological aspects of Toll like receptor 4 activation in sepsis induced acute kidney injury JO: Acta Physiol (Oxf) http://www.kidney.de/pget.php?&tw=1&pmid=27602552 #FOAvip Sepsis?induced acute kidney injury (SI?AKI) is common and associated with high mortality. Survivors are at increased risk of chronic kidney disease. The precise mechanism underlying SI?AKI is unknown, and no curative treatment exists. Toll?like receptor 4 (TLR4) activates the innate immune system in response to exogenous microbial products. The result is an inflammatory reaction aimed at clearing a potential infection. However, the consequence may also be organ dysfunction as the immune response can cause collateral damage to host tissue. The purpose of this review is to describe the basis for how ligand binding to TLR4 has the potential to cause renal dysfunction and the mechanisms by which this may take place in gram?negative sepsis. In addition, we highlight areas for future research that can further our knowledge of the pathogenesis of SI?AKI in relation to TLR4 activation. TLR4 is expressed in the kidney. Activation of TLR4 causes cytokine and chemokine release as well as renal leucocyte infiltration. It also results in endothelial and tubular dysfunction in addition to altered renal metabolism and circulation. From a physiological standpoint, inhibiting TLR4 in large animal experimental SI?AKI significantly improves renal function. Thus, current evidence indicates that TLR4 has the ability to mediate SI?AKI by a number of mechanisms. The strong experimental evidence supporting a role of TLR4 in the pathogenesis of SI?AKI in combination with the availability of pharmacological tools to target TLR4 warrants future human studies. Twit Text FOAVip Physiological aspects of Toll like receptor 4 activation in sepsis induced acute kidney injury ????Acta Physiol (Oxf) http://www.kidney.de/pget.php?&tw=1&pmid=27602552 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27602552 #FOAvip English Wikipedia <ref>{{Cite pmid|27602552}}</ref> Physiological aspects of Toll?like receptor 4 activation in sepsis?induced acute kidney injury #MMPMID27602552 Anderberg SB; Luther T; Frithiof R Acta Physiol (Oxf) 2017[Mar]; 219 (3): 573-88 PMID27602552show ga Sepsis?induced acute kidney injury (SI?AKI) is common and associated with high mortality. Survivors are at increased risk of chronic kidney disease. The precise mechanism underlying SI?AKI is unknown, and no curative treatment exists. Toll?like receptor 4 (TLR4) activates the innate immune system in response to exogenous microbial products. The result is an inflammatory reaction aimed at clearing a potential infection. However, the consequence may also be organ dysfunction as the immune response can cause collateral damage to host tissue. The purpose of this review is to describe the basis for how ligand binding to TLR4 has the potential to cause renal dysfunction and the mechanisms by which this may take place in gram?negative sepsis. In addition, we highlight areas for future research that can further our knowledge of the pathogenesis of SI?AKI in relation to TLR4 activation. TLR4 is expressed in the kidney. Activation of TLR4 causes cytokine and chemokine release as well as renal leucocyte infiltration. It also results in endothelial and tubular dysfunction in addition to altered renal metabolism and circulation. From a physiological standpoint, inhibiting TLR4 in large animal experimental SI?AKI significantly improves renal function. Thus, current evidence indicates that TLR4 has the ability to mediate SI?AKI by a number of mechanisms. The strong experimental evidence supporting a role of TLR4 in the pathogenesis of SI?AKI in combination with the availability of pharmacological tools to target TLR4 warrants future human studies. äPhysiological aspects of Toll?like receptor 4 activation in sepsis?ind(epmc).pdf DeepDyve Pubget Overpricing