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10.1038/nrneph.2016.186 http://scihub22266oqcxt.onion/10.1038/nrneph.2016.186 C5508527!5508527 !28090081     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28090081 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28090081 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Rev+Nephrol 2017 ; 13 (3 ): 143-151 Nephropedia Template TP {{tp|p=28090081 |t=2017. Metabolic reprogramming and tolerance during sepsis-induced AKI |pdf=|usr=}}{{28090081 }} gab.com Text Metabolic reprogramming and tolerance during sepsis-induced AKI JO: Nat Rev Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=28090081 #FOAvip The host defence against infection is an adaptive response in which several mechanisms are deployed to decrease the pathogen load, limit tissue injury and restore homeostasis. In the past few years new evidence has suggested that the ability of the immune system to limit the microbial burden - termed resistance - might not be the only defence mechanism. In fact, the capacity of the host to decrease its own susceptibility to inflammation- induced tissue damage - termed tolerance - might be as important as resistance in determining the outcome of the infection. Metabolic adaptations are central to the function of the cellular immune response. Coordinated reprogramming of metabolic signalling enables cells to execute resistance and tolerance pathways, withstand injury, steer tissue repair and promote organ recovery. During sepsis-induced acute kidney injury, early reprogramming of metabolism can determine the extent of organ dysfunction, progression to fibrosis, and the development of chronic kidney disease. Here we discuss the mechanisms of tolerance that act in the kidney during sepsis, with particular attention to the role of metabolic responses in coordinating these adaptive strategies. We suggest a novel conceptual model of the cellular and organic response to sepsis that might lead to new avenues for targeted, organ-protective therapies. Twit Text FOAVip Metabolic reprogramming and tolerance during sepsis-induced AKI ????Nat Rev Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=28090081 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28090081 #FOAvip English Wikipedia <ref>{{Cite pmid|28090081 }}</ref> Metabolic reprogramming and tolerance during sepsis-induced AKI #MMPMID28090081 Gómez H ; Kellum JA ; Ronco C Nat Rev Nephrol 2017[Mar]; 13 (3 ): 143-151 PMID28090081 show ga The host defence against infection is an adaptive response in which several mechanisms are deployed to decrease the pathogen load, limit tissue injury and restore homeostasis. In the past few years new evidence has suggested that the ability of the immune system to limit the microbial burden - termed resistance - might not be the only defence mechanism. In fact, the capacity of the host to decrease its own susceptibility to inflammation- induced tissue damage - termed tolerance - might be as important as resistance in determining the outcome of the infection. Metabolic adaptations are central to the function of the cellular immune response. Coordinated reprogramming of metabolic signalling enables cells to execute resistance and tolerance pathways, withstand injury, steer tissue repair and promote organ recovery. During sepsis-induced acute kidney injury, early reprogramming of metabolism can determine the extent of organ dysfunction, progression to fibrosis, and the development of chronic kidney disease. Here we discuss the mechanisms of tolerance that act in the kidney during sepsis, with particular attention to the role of metabolic responses in coordinating these adaptive strategies. We suggest a novel conceptual model of the cellular and organic response to sepsis that might lead to new avenues for targeted, organ-protective therapies. |Acute Kidney Injury/complications/*etiology/*metabolism [MESH] |Animals [MESH] |Humans [MESH] |Immune Tolerance [MESH] |Renal Insufficiency, Chronic/etiology [MESH]Metabolic reprogramming and tolerance during sepsis-induced AKI (epmc).pdf DeepDyve Pubget Overpricing