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10.1053/j.ajkd.2016.10.037 http://scihub22266oqcxt.onion/10.1053/j.ajkd.2016.10.037 C5366088!5366088!28139396     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28139396&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 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Kidney+Dis 2017 ; 69 (4): 531-45 Nephropedia Template TP {{tp|p=28139396|t=2017. Heme Oxygenase 1 as a Therapeutic Target in Acute Kidney Injury |pdf=|usr=}}{{28139396}} gab.com Text Heme Oxygenase 1 as a Therapeutic Target in Acute Kidney Injury JO: Am J Kidney Dis http://www.kidney.de/pget.php?&tw=1&pmid=28139396 #FOAvip A common clinical condition, acute kidney injury (AKI) significantly influences morbidity and mortality, particularly in critically ill patients. The pathophysiology of AKI is complex and involves multiple pathways including inflammation, autophagy, cell cycle progression, and oxidative stress. Recent evidence suggests that a single insult to the kidney significantly enhances the propensity to develop chronic kidney disease. Therefore, generation of effective therapies against AKI are timely. In this context, the cytoprotective effects of heme oxygenase 1 (HO-1) in animal models of AKI are well documented. HO-1 modulates oxidative stress, autophagy, and inflammation, and regulates the progression of cell cycle via direct and indirect mechanisms. These beneficial effects of HO-1 induction during AKI are, in part, mediated by the by-products of the HO reaction (iron, carbon monoxide, and bile pigments). This review highlights the recent advances in the molecular mechanisms of HO-1?mediated cytoprotection and discusses the translational potential of HO-1 induction in AKI. Twit Text FOAVip Heme Oxygenase 1 as a Therapeutic Target in Acute Kidney Injury ????Am J Kidney Dis http://www.kidney.de/pget.php?&tw=1&pmid=28139396 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28139396 #FOAvip English Wikipedia <ref>{{Cite pmid|28139396}}</ref> Heme Oxygenase 1 as a Therapeutic Target in Acute Kidney Injury #MMPMID28139396 Bolisetty S; Zarjou A; Agarwal A Am J Kidney Dis 2017[Apr]; 69 (4): 531-45 PMID28139396show ga A common clinical condition, acute kidney injury (AKI) significantly influences morbidity and mortality, particularly in critically ill patients. The pathophysiology of AKI is complex and involves multiple pathways including inflammation, autophagy, cell cycle progression, and oxidative stress. Recent evidence suggests that a single insult to the kidney significantly enhances the propensity to develop chronic kidney disease. Therefore, generation of effective therapies against AKI are timely. In this context, the cytoprotective effects of heme oxygenase 1 (HO-1) in animal models of AKI are well documented. HO-1 modulates oxidative stress, autophagy, and inflammation, and regulates the progression of cell cycle via direct and indirect mechanisms. These beneficial effects of HO-1 induction during AKI are, in part, mediated by the by-products of the HO reaction (iron, carbon monoxide, and bile pigments). This review highlights the recent advances in the molecular mechanisms of HO-1?mediated cytoprotection and discusses the translational potential of HO-1 induction in AKI. äHeme Oxygenase 1 as a Therapeutic Target in Acute Kidney Injury (epmc).pdf DeepDyve Pubget Overpricing