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10.1073/pnas.1305538110 http://scihub22266oqcxt.onion/10.1073/pnas.1305538110 23818611!3718149!23818611     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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\23818611.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Proc+Natl+Acad+Sci+U+S+A 2013 ; 110 (29): 12024-9 Nephropedia Template TP {{tp|p=23818611|t=2013. Two independent pathways of regulated necrosis mediate ischemia-reperfusion injury |pdf=|usr=}}{{23818611}} gab.com Text Two independent pathways of regulated necrosis mediate ischemia-reperfusion injury JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=23818611 #FOAvip Regulated necrosis (RN) may result from cyclophilin (Cyp)D-mediated mitochondrial permeability transition (MPT) and receptor-interacting protein kinase (RIPK)1-mediated necroptosis, but it is currently unclear whether there is one common pathway in which CypD and RIPK1 act in or whether separate RN pathways exist. Here, we demonstrate that necroptosis in ischemia-reperfusion injury (IRI) in mice occurs as primary organ damage, independent of the immune system, and that mice deficient for RIPK3, the essential downstream partner of RIPK1 in necroptosis, are protected from IRI. Protection of RIPK3-knockout mice was significantly stronger than of CypD-deficient mice. Mechanistically, in vivo analysis of cisplatin-induced acute kidney injury and hyperacute TNF-shock models in mice suggested the distinctness of CypD-mediated MPT from RIPK1/RIPK3-mediated necroptosis. We, therefore, generated CypD-RIPK3 double-deficient mice that are viable and fertile without an overt phenotype and that survived prolonged IRI, which was lethal to each single knockout. Combined application of the RIPK1 inhibitor necrostatin-1 and the MPT inhibitor sanglifehrin A confirmed the results with mutant mice. The data demonstrate the pathophysiological coexistence and corelevance of two separate pathways of RN in IRI and suggest that combination therapy targeting distinct RN pathways can be beneficial in the treatment of ischemic injury. Twit Text FOAVip Two independent pathways of regulated necrosis mediate ischemia-reperfusion injury ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=23818611 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23818611 #FOAvip English Wikipedia <ref>{{Cite pmid|23818611}}</ref> Two independent pathways of regulated necrosis mediate ischemia-reperfusion injury #MMPMID23818611 Linkermann A; Brasen JH; Darding M; Jin MK; Sanz AB; Heller JO; De Zen F; Weinlich R; Ortiz A; Walczak H; Weinberg JM; Green DR; Kunzendorf U; Krautwald S Proc Natl Acad Sci U S A 2013[Jul]; 110 (29): 12024-9 PMID23818611show ga Regulated necrosis (RN) may result from cyclophilin (Cyp)D-mediated mitochondrial permeability transition (MPT) and receptor-interacting protein kinase (RIPK)1-mediated necroptosis, but it is currently unclear whether there is one common pathway in which CypD and RIPK1 act in or whether separate RN pathways exist. Here, we demonstrate that necroptosis in ischemia-reperfusion injury (IRI) in mice occurs as primary organ damage, independent of the immune system, and that mice deficient for RIPK3, the essential downstream partner of RIPK1 in necroptosis, are protected from IRI. Protection of RIPK3-knockout mice was significantly stronger than of CypD-deficient mice. Mechanistically, in vivo analysis of cisplatin-induced acute kidney injury and hyperacute TNF-shock models in mice suggested the distinctness of CypD-mediated MPT from RIPK1/RIPK3-mediated necroptosis. We, therefore, generated CypD-RIPK3 double-deficient mice that are viable and fertile without an overt phenotype and that survived prolonged IRI, which was lethal to each single knockout. Combined application of the RIPK1 inhibitor necrostatin-1 and the MPT inhibitor sanglifehrin A confirmed the results with mutant mice. The data demonstrate the pathophysiological coexistence and corelevance of two separate pathways of RN in IRI and suggest that combination therapy targeting distinct RN pathways can be beneficial in the treatment of ischemic injury. |Animals[MESH] |Apoptosis/*physiology[MESH] |Cell Line[MESH] |Cyclophilins/genetics/*metabolism[MESH] |DNA Primers/genetics[MESH] |Genotype[MESH] |Kaplan-Meier Estimate[MESH] |L-Lactate Dehydrogenase/metabolism[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Mitochondrial Membrane Transport Proteins/*metabolism[MESH] |Mitochondrial Permeability Transition Pore[MESH] |Necrosis/etiology/*physiopathology[MESH] |Peptidyl-Prolyl Isomerase F[MESH] |Receptor-Interacting Protein Serine-Threonine Kinases/genetics/*metabolism[MESH]Two independent pathways of regulated necrosis mediate ischemia-reperf(epmc).pdf DeepDyve Pubget Overpricing