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@ARTICLE{Papathanasiou:127270,
      author       = {S. Papathanasiou and S. Rickelt$^*$ and M. E. Soriano and
                      T. G. Schips and H. J. Maier and C. H. Davos and A. Varela
                      and L. Kaklamanis and D. L. Mann and Y. Capetanaki},
      title        = {{T}umor necrosis factor-α confers cardioprotection through
                      ectopic expression of keratins {K}8 and {K}18.},
      journal      = {Nature medicine},
      volume       = {21},
      number       = {9},
      issn         = {1546-170X},
      address      = {New York, NY},
      publisher    = {Nature America Inc.},
      reportid     = {DKFZ-2017-03295},
      pages        = {1076 - 1084},
      year         = {2015},
      abstract     = {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.},
      keywords     = {Desmin (NLM Chemicals) / Keratin-18 (NLM Chemicals) /
                      Keratin-8 (NLM Chemicals) / NF-kappa B (NLM Chemicals) /
                      Tumor Necrosis Factor-alpha (NLM Chemicals)},
      cin          = {A991},
      ddc          = {610},
      cid          = {I:(DE-He78)A991-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26280121},
      pmc          = {pmc:PMC5419049},
      doi          = {10.1038/nm.3925},
      url          = {https://inrepo02.dkfz.de/record/127270},
}