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@ARTICLE{Kumar:166280,
      author       = {V. Kumar and R. Agrawal and A. Pandey and S. Kopf and M.
                      Hoeffgen and S. Kaymak and O. R. Bandapalli$^*$ and V.
                      Gorbunova and A. Seluanov and M. A. Mall and S. Herzig and
                      P. P. Nawroth},
      title        = {{C}ompromised {DNA} repair is responsible for
                      diabetes-associated fibrosis.},
      journal      = {The EMBO journal},
      volume       = {39},
      number       = {11},
      issn         = {1460-2075},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DKFZ-2020-02773},
      pages        = {e103477},
      year         = {2020},
      note         = {2020 Jun 2;39(11):e103477},
      abstract     = {Diabetes-associated organ fibrosis, marked by elevated
                      cellular senescence, is a growing health concern.
                      Intriguingly, the mechanism underlying this association
                      remained unknown. Moreover, insulin alone can neither
                      reverse organ fibrosis nor the associated secretory
                      phenotype, favoring the exciting notion that thus far
                      unknown mechanisms must be operative. Here, we show that
                      experimental type 1 and type 2 diabetes impairs DNA repair,
                      leading to senescence, inflammatory phenotypes, and
                      ultimately fibrosis. Carbohydrates were found to trigger
                      this cascade by decreasing the NAD+ /NADH ratio and
                      NHEJ-repair in vitro and in diabetes mouse models.
                      Restoring DNA repair by nuclear over-expression of
                      phosphomimetic RAGE reduces DNA damage, inflammation, and
                      fibrosis, thereby restoring organ function. Our study
                      provides a novel conceptual framework for understanding
                      diabetic fibrosis on the basis of persistent DNA damage
                      signaling and points to unprecedented approaches to restore
                      DNA repair capacity for resolution of fibrosis in patients
                      with diabetes.},
      keywords     = {DNA double-strand breaks (Other) / diabetes (Other) /
                      nuclear isoform of the Receptor for Advanced Glycation End
                      products (Other) / pulmonary fibrosis (Other) / reducing
                      carbohydrates (Other)},
      cin          = {B062},
      ddc          = {570},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32338774},
      pmc          = {pmc:PMC7265245},
      doi          = {10.15252/embj.2019103477},
      url          = {https://inrepo02.dkfz.de/record/166280},
}