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@ARTICLE{Berulava:141698,
      author       = {Berulava, Tea and Buchholz, Eric and Elerdashvili, Vakhtang
                      and Pena Centeno, Tonatiuh and Islam, Rezaul and Lbik, Dawid
                      and Mohamed, Belal A and Renner, Andre and von Lewinski,
                      Dirk and Sacherer, Michael and Bohnsack, Katherine E and
                      Bohnsack, Markus T and Jain, Gaurav and Capece, Vincenzo and
                      Cleve, Nicole and Burkhardt, Susanne and Hasenfuss, Gerd and
                      Fischer, Andre and Toischer, Karl},
      title        = {{C}hanges in m6{A} {RNA} methylation contribute to heart
                      failure progression by modulating translation.},
      journal      = {European journal of heart failure},
      volume       = {22},
      number       = {1},
      issn         = {1388-9842},
      address      = {Oxford},
      publisher    = {Wiley},
      reportid     = {DZNE-2020-00029},
      pages        = {54-66},
      year         = {2020},
      abstract     = {Deregulation of epigenetic processes and aberrant gene
                      expression are important mechanisms in heart failure. Here
                      we studied the potential relevance of m6A RNA methylation in
                      heart failure development.We analysed m6A RNA methylation
                      via next-generation sequencing. We found that approximately
                      one quarter of the transcripts in the healthy mouse and
                      human heart exhibit m6A RNA methylation. During progression
                      to heart failure we observed that changes in m6A RNA
                      methylation exceed changes in gene expression both in mouse
                      and human. RNAs with altered m6A RNA methylation were mainly
                      linked to metabolic and regulatory pathways, while changes
                      in RNA expression level mainly represented changes in
                      structural plasticity. Mechanistically, we could link m6A
                      RNA methylation to altered RNA translation and protein
                      production. Interestingly, differentially methylated but not
                      differentially expressed RNAs showed differential polysomal
                      occupancy, indicating transcription-independent modulation
                      of translation. Furthermore, mice with a cardiomyocyte
                      restricted knockout of the RNA demethylase Fto exhibited an
                      impaired cardiac function compared to control mice.We could
                      show that m6A landscape is altered in heart hypertrophy and
                      heart failure. m6A RNA methylation changes lead to changes
                      in protein abundance, unconnected to mRNA levels. This
                      uncovers a new transcription-independent mechanisms of
                      translation regulation. Therefore, our data suggest that
                      modulation of epitranscriptomic processes such as m6A
                      methylation might be an interesting target for therapeutic
                      interventions.},
      keywords     = {Animals / Epigenesis, Genetic / Heart Failure: genetics /
                      Methylation / Mice / RNA: genetics / RNA: metabolism / RNA,
                      Messenger: genetics},
      cin          = {AG Fischer 1 ; AG Fischer / Göttingen common /
                      Bioinformatics and Genome Dynamics Core / AG Bonn 2 ; AG
                      Bonn 2 / RNAome database},
      ddc          = {610},
      cid          = {I:(DE-2719)1410002 / I:(DE-2719)6000014 /
                      I:(DE-2719)1440016 / I:(DE-2719)1440012 /
                      I:(DE-2719)1410004},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31849158},
      doi          = {10.1002/ejhf.1672},
      url          = {https://pub.dzne.de/record/141698},
}