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10.1681/ASN.2016070761 http://scihub22266oqcxt.onion/10.1681/ASN.2016070761 C5407729!5407729 !27881606     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 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\27881606 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Am+Soc+Nephrol 2017 ; 28 (5 ): 1437-1449 Nephropedia Template TP {{tp|p=27881606 |t=2017. Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1? and IL-18 and Arrests CKD |pdf=|usr=}}{{27881606 }} gab.com Text Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1 and IL-18 and Arrests CKD JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=27881606 #FOAvip The innate immune system has been implicated in both AKI and CKD. Damaged mitochondria release danger molecules, such as reactive oxygen species, DNA, and cardiolipin, which can cause NLRP3 inflammasome activation and upregulation of IL-18 and IL-1? It is not known if mitochondrial damage persists long after ischemia to sustain chronic inflammasome activation. We conducted a 9-month study in Sprague-Dawley rats after 45 minutes of bilateral renal ischemia. We detected glomerular and peritubular capillary rarefaction, macrophage infiltration, and fibrosis at 1 month. Transmission electron microscopy revealed mitochondrial degeneration, mitophagy, and deformed foot processes in podocytes. These changes progressed over the study period, with a persistent increase in renal cortical expression of IL-18, IL-1?, and TGF-?, despite a gradual decline in TNF-? expression and macrophage infiltration. Treatment with a mitoprotective agent (SS-31; elamipretide) for 6 weeks, starting 1 month after ischemia, preserved mitochondrial integrity, ameliorated expression levels of all inflammatory markers, restored glomerular capillaries and podocyte structure, and arrested glomerulosclerosis and interstitial fibrosis. Further, helium ion microscopy vividly demonstrated the restoration of podocyte structure by SS-31. The protection by SS-31 was sustained for ?6 months after treatment ended, with normalization of IL-18 and IL-1? expression. These results support a role for mitochondrial damage in inflammasome activation and CKD and suggest mitochondrial protection as a novel therapeutic approach that can arrest the progression of CKD. Notably, SS-31 is effective when given long after AKI and provides persistent protection after termination of drug treatment. Twit Text FOAVip Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1 and IL-18 and Arrests CKD ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=27881606 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27881606 #FOAvip English Wikipedia <ref>{{Cite pmid|27881606 }}</ref> Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1? and IL-18 and Arrests CKD #MMPMID27881606 Szeto HH ; Liu S ; Soong Y ; Seshan SV ; Cohen-Gould L ; Manichev V ; Feldman LC ; Gustafsson T J Am Soc Nephrol 2017[May]; 28 (5 ): 1437-1449 PMID27881606 show ga The innate immune system has been implicated in both AKI and CKD. Damaged mitochondria release danger molecules, such as reactive oxygen species, DNA, and cardiolipin, which can cause NLRP3 inflammasome activation and upregulation of IL-18 and IL-1? It is not known if mitochondrial damage persists long after ischemia to sustain chronic inflammasome activation. We conducted a 9-month study in Sprague-Dawley rats after 45 minutes of bilateral renal ischemia. We detected glomerular and peritubular capillary rarefaction, macrophage infiltration, and fibrosis at 1 month. Transmission electron microscopy revealed mitochondrial degeneration, mitophagy, and deformed foot processes in podocytes. These changes progressed over the study period, with a persistent increase in renal cortical expression of IL-18, IL-1?, and TGF-?, despite a gradual decline in TNF-? expression and macrophage infiltration. Treatment with a mitoprotective agent (SS-31; elamipretide) for 6 weeks, starting 1 month after ischemia, preserved mitochondrial integrity, ameliorated expression levels of all inflammatory markers, restored glomerular capillaries and podocyte structure, and arrested glomerulosclerosis and interstitial fibrosis. Further, helium ion microscopy vividly demonstrated the restoration of podocyte structure by SS-31. The protection by SS-31 was sustained for ?6 months after treatment ended, with normalization of IL-18 and IL-1? expression. These results support a role for mitochondrial damage in inflammasome activation and CKD and suggest mitochondrial protection as a novel therapeutic approach that can arrest the progression of CKD. Notably, SS-31 is effective when given long after AKI and provides persistent protection after termination of drug treatment. |Acute Disease [MESH] |Animals [MESH] |Interleukin-18/*physiology [MESH] |Interleukin-1beta/*physiology [MESH] |Ischemia/*complications [MESH] |Kidney/*blood supply [MESH] |Male [MESH] |Mitochondria/*drug effects/*physiology [MESH] |Oligopeptides/*pharmacology/*therapeutic use [MESH] |Podocytes/drug effects [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Renal Insufficiency, Chronic/*etiology/*prevention & control [MESH] |Time Factors [MESH]Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregu(epmc).pdf DeepDyve Pubget Overpricing