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@ARTICLE{Sieckmann:281535,
      author       = {Sieckmann, Katharina and Winnerling, Nora and Silva
                      Ribeiro, Dalila Juliana and Yüksel, Seniz and Kardinal,
                      Ronja and Steinheuer, Lisa Maria and Frechen, Fabian and
                      Corrêa, Luis Henrique and Schermann, Geza and Klausen,
                      Christina and Blank-Stein, Nelli and Schulte-Schrepping,
                      Jonas and Osei-Sarpong, Collins and Becker, Matthias and
                      Bonaguro, Lorenzo and Beyer, Marc and May-Simera, Helen
                      Louise and Zurkovic, Jelena and Thiele, Christoph and
                      Thurley, Kevin and Sorokin, Lydia and Ruiz de Almodovar,
                      Carmen and Mass, Elvira and Wachten, Dagmar},
      title        = {{BBS}8-dependent ciliary {H}edgehog signaling governs cell
                      fate in the white adipose tissue.},
      journal      = {The EMBO journal},
      volume       = {44},
      number       = {19},
      issn         = {0261-4189},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DZNE-2025-01153},
      pages        = {5315 - 5336},
      year         = {2025},
      abstract     = {The primary cilium plays a crucial role in regulating
                      whole-body energy metabolism, as reflected in Bardet-Biedl
                      syndrome (BBS), where ciliary dysfunction leads to obesity
                      due to hyperphagia and white adipose tissue (WAT)
                      remodeling. Regulation of the fate and differentiation of
                      adipocyte precursor cells (APCs) is essential for
                      maintaining WAT homeostasis during obesity. Using Bbs8-/-
                      mice that recapitulate the BBS patient phenotype, we
                      demonstrate that primary cilia dysfunction reduces the
                      stem-cell-like P1 APC subpopulation by inducing a phenotypic
                      switch to a fibrogenic progenitor state. This switch is
                      characterized by extracellular matrix (ECM) remodeling and
                      upregulation of the fibrosis marker CD9, even before the
                      onset of obesity. Single-cell RNA sequencing reveals a
                      direct transition of P1 APCs into fibrogenic progenitors,
                      bypassing the committed P2 progenitor state. Ectopic ciliary
                      Hedgehog signaling upon loss of BBS8 appears as a central
                      driver of the molecular changes in Bbs8-/- APCs, altering
                      their differentiation into adipocytes and promoting their
                      lipid uptake. These findings unravel a novel role for
                      primary cilia in governing APC fate by determining the
                      balance between adipogenesis and fibrogenesis, and suggest
                      potential therapeutic targets for obesity.},
      keywords     = {Animals / Adipose Tissue, White: metabolism / Adipose
                      Tissue, White: cytology / Adipose Tissue, White: pathology /
                      Mice / Hedgehog Proteins: metabolism / Hedgehog Proteins:
                      genetics / Signal Transduction / Cilia: metabolism / Mice,
                      Knockout / Cell Differentiation / Adipogenesis /
                      Bardet-Biedl Syndrome: metabolism / Bardet-Biedl Syndrome:
                      genetics / Bardet-Biedl Syndrome: pathology / Obesity:
                      metabolism / Obesity: genetics / Obesity: pathology /
                      Adipocytes: metabolism / Adipocytes: cytology /
                      Microtubule-Associated Proteins: metabolism /
                      Microtubule-Associated Proteins: genetics / Adipose Tissue
                      (Other) / BBS (Other) / Cell Fate (Other) / Cilia (Other) /
                      Hedgehog Proteins (NLM Chemicals) / Microtubule-Associated
                      Proteins (NLM Chemicals)},
      cin          = {AG Schultze / AG Beyer / AG Becker / AG Bonaguro},
      ddc          = {570},
      cid          = {I:(DE-2719)1013038 / I:(DE-2719)1013035 /
                      I:(DE-2719)5000079 / I:(DE-2719)1016005},
      pnm          = {354 - Disease Prevention and Healthy Aging (POF4-354) / 351
                      - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-354 / G:(DE-HGF)POF4-351},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40836034},
      pmc          = {pmc:PMC12489102},
      doi          = {10.1038/s44318-025-00524-y},
      url          = {https://pub.dzne.de/record/281535},
}