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@ARTICLE{Zioni:275374,
      author       = {N. Zioni and A. A. Bercovich and N. Chapal-Ilani and T.
                      Bacharach and N. Rappoport and A. Solomon and R. Avraham and
                      E. Kopitman and Z. Porat and M. Sacma and G. Hartmut and M.
                      Scheller and C. Müller-Tidow$^*$ and D. Lipka$^*$ and E.
                      Shlush and M. Minden and N. Kaushansky and L. I. Shlush},
      title        = {{I}nflammatory signals from fatty bone marrow support
                      {DNMT}3{A} driven clonal hematopoiesis.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-00740},
      pages        = {2070},
      year         = {2023},
      abstract     = {Both fatty bone marrow (FBM) and somatic mutations in
                      hematopoietic stem cells (HSCs), also termed clonal
                      hematopoiesis (CH) accumulate with human aging. However it
                      remains unclear whether FBM can modify the evolution of CH.
                      To address this question, we herein present the interaction
                      between CH and FBM in two preclinical male mouse models:
                      after sub-lethal irradiation or after castration. An
                      adipogenesis inhibitor (PPARγ inhibitor) is used in both
                      models as a control. A significant increase in self-renewal
                      can be detected in both human and rodent DNMT3AMut-HSCs when
                      exposed to FBM. DNMT3AMut-HSCs derived from older mice
                      interacting with FBM have even higher self-renewal in
                      comparison to DNMT3AMut-HSCs derived from younger mice.
                      Single cell RNA-sequencing on rodent HSCs after exposing
                      them to FBM reveal a 6-10 fold increase in DNMT3AMut-HSCs
                      and an activated inflammatory signaling. Cytokine analysis
                      of BM fluid and BM derived adipocytes grown in vitro
                      demonstrates an increased IL-6 levels under FBM conditions.
                      Anti-IL-6 neutralizing antibodies significantly reduce the
                      selective advantage of DNMT3AMut-HSCs exposed to FBM.
                      Overall, paracrine FBM inflammatory signals promote
                      DNMT3A-driven clonal hematopoiesis, which can be inhibited
                      by blocking the IL-6 pathway.},
      cin          = {A350 / B340 / HD01},
      ddc          = {500},
      cid          = {I:(DE-He78)A350-20160331 / I:(DE-He78)B340-20160331 /
                      I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37045808},
      doi          = {10.1038/s41467-023-36906-1},
      url          = {https://inrepo02.dkfz.de/record/275374},
}