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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Weinberg, Joel M. Darding, Maurice Krautwald, Stefan Kunzendorf, Ulrich Linkermann, Andreas Heller, Jan-ole Sanz, Ana B. Weinlich, Ricardo Green, Douglas R. Jin, Mi Kyung Walczak, Henning Bräsen, Jan Hinrich Ortiz, Alberto De Zen, Federica |
| Description | Author Affiliation: Linkermann A ( Division of Nephrology and Hypertension and Institute for Pathology, Christian-Albrechts-University, 24105 Kiel, Germany.); |
| Abstract | 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. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 29 |
| Volume Number | 110 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2013-07-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Apoptosis Physiology Cyclophilins Metabolism Mitochondrial Membrane Transport Proteins Necrosis Physiopathology Receptor-Interacting Protein Serine-Threonine Kinases Reperfusion Injury Complications Animals Cell Line Genetics DNA Primers Genotype Kaplan-Meier Estimate L-Lactate Dehydrogenase Mice Mice, Inbred C57BL Mice, Knockout Etiology Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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