001     127270
005     20240228140915.0
024 7 _ |a 10.1038/nm.3925
|2 doi
024 7 _ |a pmid:26280121
|2 pmid
024 7 _ |a pmc:PMC5419049
|2 pmc
024 7 _ |a 1078-8956
|2 ISSN
024 7 _ |a 1546-170X
|2 ISSN
024 7 _ |a altmetric:4405412
|2 altmetric
037 _ _ |a DKFZ-2017-03295
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Papathanasiou, Stamatis
|0 P:(DE-HGF)0
|b 0
245 _ _ |a Tumor necrosis factor-α confers cardioprotection through ectopic expression of keratins K8 and K18.
260 _ _ |a New York, NY
|c 2015
|b Nature America Inc.
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1508309346_2417
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Tumor necrosis factor-α (TNF-α), one of the major stress-induced proinflammatory cytokines, is upregulated in the heart after tissue injury, and its sustained expression can contribute to the development of heart failure. Whether TNF-α also exerts cytoprotective effects in heart failure is not known. Here we provide evidence for a cardioprotective function of TNF-α in a genetic heart failure model, desmin-deficient mice. The cardioprotective effects of TNF-α are a consequence of nuclear factor-κB (NF-κB)-mediated ectopic expression in cardiomyocytes of keratin 8 (K8) and keratin 18 (K18), two epithelial-specific intermediate filament proteins. In cardiomyocytes, K8 and K18 (K8/K18) formed an alternative cytoskeletal network that localized mainly at intercalated discs (IDs) and conferred cardioprotection by maintaining normal ID structure and mitochondrial integrity and function. Ectopic induction of K8/K18 expression in cardiomyocytes also occurred in other genetic and experimental models of heart failure. Loss of the K8/K18 network resulted in a maladaptive cardiac phenotype following transverse aortic constriction. In human failing myocardium, where TNF-α expression is upregulated, K8/K18 were also ectopically expressed and localized primarily at IDs, which did not contain detectable amounts of desmin. Thus, TNF-α- and NF-κB-mediated formation of an alternative, stress-induced intermediate filament cytoskeleton has cardioprotective function in mice and potentially in humans.
536 _ _ |a 311 - Signalling pathways, cell and tumor biology (POF3-311)
|0 G:(DE-HGF)POF3-311
|c POF3-311
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Desmin
|2 NLM Chemicals
650 _ 7 |a Keratin-18
|2 NLM Chemicals
650 _ 7 |a Keratin-8
|2 NLM Chemicals
650 _ 7 |a NF-kappa B
|2 NLM Chemicals
650 _ 7 |a Tumor Necrosis Factor-alpha
|2 NLM Chemicals
700 1 _ |a Rickelt, Steffen
|0 P:(DE-HGF)0
|b 1
700 1 _ |a Soriano, Maria Eugenia
|b 2
700 1 _ |a Schips, Tobias G
|b 3
700 1 _ |a Maier, Harald J
|b 4
700 1 _ |a Davos, Constantinos H
|b 5
700 1 _ |a Varela, Aimilia
|b 6
700 1 _ |a Kaklamanis, Loukas
|b 7
700 1 _ |a Mann, Douglas L
|b 8
700 1 _ |a Capetanaki, Yassemi
|b 9
773 _ _ |a 10.1038/nm.3925
|g Vol. 21, no. 9, p. 1076 - 1084
|0 PERI:(DE-600)1484517-9
|n 9
|p 1076 - 1084
|t Nature medicine
|v 21
|y 2015
|x 1546-170X
909 C O |o oai:inrepo02.dkfz.de:127270
|p VDB
910 1 _ |a External Institute
|0 I:(DE-HGF)0
|k Extern
|b 0
|6 P:(DE-HGF)0
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 1
|6 P:(DE-HGF)0
913 1 _ |a DE-HGF
|l Krebsforschung
|1 G:(DE-HGF)POF3-310
|0 G:(DE-HGF)POF3-311
|2 G:(DE-HGF)POF3-300
|v Signalling pathways, cell and tumor biology
|x 0
|4 G:(DE-HGF)POF
|3 G:(DE-HGF)POF3
|b Gesundheit
914 1 _ |y 2015
915 _ _ |a Nationallizenz
|0 StatID:(DE-HGF)0420
|2 StatID
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0310
|2 StatID
|b NCBI Molecular Biology Database
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b NAT MED : 2015
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Thomson Reuters Master Journal List
915 _ _ |a WoS
|0 StatID:(DE-HGF)0110
|2 StatID
|b Science Citation Index
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
915 _ _ |a WoS
|0 StatID:(DE-HGF)0111
|2 StatID
|b Science Citation Index Expanded
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1110
|2 StatID
|b Current Contents - Clinical Medicine
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
915 _ _ |a IF >= 30
|0 StatID:(DE-HGF)9930
|2 StatID
|b NAT MED : 2015
920 1 _ |0 I:(DE-He78)A991-20160331
|k A991
|l Helmholtz-Professur Zellbiologie
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a I:(DE-He78)A991-20160331
980 _ _ |a UNRESTRICTED


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21