% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Hasan:302263,
      author       = {S. S. Hasan and D. John and M. Rudnicki and I. AlZaim and
                      D. Eberhard and I. Moll$^*$ and J. Taylor$^*$ and C. Klein
                      and M. von Heesen and L.-C. Conradi and R. H. Adams and E.
                      Lammert and J. Kalucka and C. Ruhrberg and S. Dimmeler and
                      A. Fischer},
      title        = {{O}besity drives depot-specific vascular remodeling in male
                      white adipose tissue.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01289},
      pages        = {5392},
      year         = {2025},
      note         = {Division Vascular Signaling and Cancer},
      abstract     = {Obesity-driven pathological expansion of white adipose
                      tissue (WAT) is a key driver of endothelial dysfunction.
                      However, early vascular alterations associated with
                      over-nutrition also serve to exacerbate WAT dysfunction.
                      Here, we conduct a single-cell transcriptomic analysis of
                      WAT endothelium to delineate endothelial heterogeneity and
                      elucidate vascular alterations and its consequence in a male
                      murine model of obesity. We demarcate depot-specific
                      differences in subcutaneous (sWAT) and visceral WAT (vWAT)
                      endothelium through in sillico analysis and further
                      corroboration of our findings. Moreover, we identify a
                      sWAT-specific fenestrated endothelial cell (EC) subtype,
                      which declines in obese conditions. Utilizing systemic
                      anti-VEGFA blockade and genetic Vegfa manipulation, we
                      demonstrate that VEGFA is necessary for maintaining
                      fenestration in sWAT. Additionally, we detect this
                      fenestrated EC subtype in male human WAT, which undergoes
                      reduction in individuals with obesity. Collectively, this
                      atlas serves as a valuable tool for future studies to
                      decipher the functional significance of different WAT EC
                      subtypes.},
      keywords     = {Animals / Male / Obesity: metabolism / Obesity: pathology /
                      Obesity: genetics / Adipose Tissue, White: metabolism /
                      Adipose Tissue, White: pathology / Adipose Tissue, White:
                      blood supply / Mice / Vascular Remodeling: genetics /
                      Vascular Remodeling: physiology / Humans / Endothelial
                      Cells: metabolism / Endothelial Cells: pathology / Vascular
                      Endothelial Growth Factor A: metabolism / Vascular
                      Endothelial Growth Factor A: genetics / Vascular Endothelial
                      Growth Factor A: antagonists $\&$ inhibitors / Mice, Inbred
                      C57BL / Subcutaneous Fat: metabolism / Subcutaneous Fat:
                      pathology / Subcutaneous Fat: blood supply / Single-Cell
                      Analysis / Disease Models, Animal / Intra-Abdominal Fat:
                      metabolism / Endothelium, Vascular: metabolism /
                      Endothelium, Vascular: pathology / Vascular Endothelial
                      Growth Factor A (NLM Chemicals)},
      cin          = {A270},
      ddc          = {500},
      cid          = {I:(DE-He78)A270-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40562785},
      doi          = {10.1038/s41467-025-60910-2},
      url          = {https://inrepo02.dkfz.de/record/302263},
}