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@ARTICLE{Wanner:310355,
      author       = {N. Wanner and J. Keller and N. Liaukouskaya and G. Andrieux
                      and S. D. Laufer and M. Rogg and T. Bork and W. Liang and F.
                      Braun and F. Haas and M. N. Wong and V. G. Puelles and S. E.
                      Gies and C. Meyer and M. Boerries$^*$ and M. Helmstädter
                      and O. Kretz and I. Hild and E. Metzger$^*$ and R. Schüle
                      and W. Bechtel-Walz and T. B. Huber},
      title        = {{L}ysine-specific histone demethylase 1a regulates nephron
                      development and long-term transcriptional programming.},
      journal      = {JCI insight},
      volume       = {11},
      number       = {5},
      issn         = {2379-3708},
      address      = {Ann Arbor, Michigan},
      publisher    = {JCI Insight},
      reportid     = {DKFZ-2026-00555},
      pages        = {e190283},
      year         = {2026},
      abstract     = {Low nephron endowment constitutes a risk factor for
                      hypertension and renal disease. Epigenetic regulation is
                      crucial for nephron progenitor cell differentiation,
                      affecting nephron number and renal function. The role of
                      many epigenetic modulators, such as Lysine-specific histone
                      demethylase 1a (LSD1 or KDM1A), remains unclear. We used
                      Kdm1a-KO mice to demonstrate that Kdm1a depletion in nephron
                      progenitor cells results in reduced kidney size in neonates
                      and led to glomerulosclerosis, proteinuria, and renal cysts
                      in adults. Notably, Kdm1a deletion in podocytes or tubular
                      cells did not replicate these effects. CRISPR/Cas9-mediated
                      KDM1A deletion in human kidney organoids caused cyst
                      formation and altered gene expression, with snRNA-seq
                      revealing downregulation of podocyte genes and upregulation
                      of metabolic genes. The presence of noncoding RNAs indicated
                      roles in cell proliferation. Our study reveals the critical
                      role of Kdm1a function in nephron development and highlights
                      its affect on transcriptional programming for long-term
                      renal function and susceptibility to cyst formation.},
      keywords     = {Animals / Nephrons: growth $\&$ development / Nephrons:
                      metabolism / Nephrons: pathology / Mice / Mice, Knockout /
                      Histone Demethylases: genetics / Histone Demethylases:
                      metabolism / Humans / Podocytes: metabolism / Cell
                      Differentiation: genetics / Cell Proliferation: genetics /
                      Gene Expression Regulation, Developmental / Male /
                      Epigenesis, Genetic / Organoids / Chronic kidney disease
                      (Other) / Development (Other) / Epigenetics (Other) /
                      Nephrology (Other) / KDM1a protein, mouse (NLM Chemicals) /
                      Histone Demethylases (NLM Chemicals) / KDM1A protein, human
                      (NLM Chemicals)},
      cin          = {FR01},
      ddc          = {610},
      cid          = {I:(DE-He78)FR01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41797715},
      doi          = {10.1172/jci.insight.190283},
      url          = {https://inrepo02.dkfz.de/record/310355},
}