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@ARTICLE{Islam:157715,
      author       = {Islam, Rezaul and Lbik, Dawid and Sakib, M Sadman and
                      Maximilian Hofmann, Raoul and Berulava, Tea and Jiménez
                      Mausbach, Martí and Cha, Julia and Goldberg, Maria and
                      Elerdashvili, Vakhtang and Schiffmann, Christian and
                      Zieseniss, Anke and Katschinski, Dörthe Magdalena and
                      Sananbenesi, Farahnaz and Toischer, Karl and Fischer, Andre},
      title        = {{E}pigenetic gene expression links heart failure to memory
                      impairment.},
      journal      = {EMBO molecular medicine},
      volume       = {13},
      number       = {3},
      issn         = {1757-4684},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DZNE-2021-01172},
      pages        = {e11900},
      year         = {2021},
      abstract     = {In current clinical practice, care of diseased patients is
                      often restricted to separated disciplines. However, such an
                      organ-centered approach is not always suitable. For example,
                      cognitive dysfunction is a severe burden in heart failure
                      patients. Moreover, these patients have an increased risk
                      for age-associated dementias. The underlying molecular
                      mechanisms are presently unknown, and thus, corresponding
                      therapeutic strategies to improve cognition in heart failure
                      patients are missing. Using mice as model organisms, we show
                      that heart failure leads to specific changes in hippocampal
                      gene expression, a brain region intimately linked to
                      cognition. These changes reflect increased cellular stress
                      pathways which eventually lead to loss of neuronal
                      euchromatin and reduced expression of a hippocampal gene
                      cluster essential for cognition. Consequently, mice
                      suffering from heart failure exhibit impaired memory
                      function. These pathological changes are ameliorated via the
                      administration of a drug that promotes neuronal euchromatin
                      formation. Our study provides first insight to the molecular
                      processes by which heart failure contributes to neuronal
                      dysfunction and point to novel therapeutic avenues to treat
                      cognitive defects in heart failure patients.},
      keywords     = {Animals / Cognition / Epigenesis, Genetic / Gene Expression
                      / Heart Failure: genetics / Humans / Memory Disorders / Mice
                      / cognition (Other) / epigenetics (Other) / heart failure
                      (Other) / histone (Other) / memory impairment (Other)},
      cin          = {AG Fischer 1},
      ddc          = {610},
      cid          = {I:(DE-2719)1410002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33471428},
      pmc          = {pmc:PMC7933944},
      doi          = {10.15252/emmm.201911900},
      url          = {https://pub.dzne.de/record/157715},
}