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Cited by 554

The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.

Two independent pathways of regulated necrosis mediate ischemia–reperfusion injury

Open access
Linkermann, Andreas, Bräsen, Jan Hinrich, Darding, Maurice, Jin, Mi Kyung, Sanz, Ana B., Heller, Jan-Ole, De Zen, Federica, Weinlich, Ricardo, Ortiz, Alberto, Walczak, Henning, Weinberg, Joel M., Green, Douglas R., Kunzendorf, Ulrich, Krautwald, Stefan·2013·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.1305538110
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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.

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Show all 16 references

Research works printed but not linked: 38

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Cited by

Metadata

Authors
Linkermann, A., Bräsen, J. H., Darding, M., Jin, M. K., Sanz, A. B., Heller, J.-O., De Zen, F., Weinlich, R., Ortiz, A., Walczak, H., Weinberg, J. M., Green, D. R., Kunzendorf, U., & Krautwald, S.
Venue
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Published
2013-07
Volume
110
Issue
29
Pages
12024-12029
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.1305538110
OpenAlex
W1991997670
Cited by
554
References
16
FWCI
20.58
Type
journal article
Language
en
Open access
bronze

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