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@ARTICLE{Schwarz:294070,
      author       = {D. Schwarz and M. L. Marois and V. Sturm and A. S. Peters
                      and R. Longuespée$^*$ and D. Helm$^*$ and M. Schneider$^*$
                      and B. Eichmüller and A. S. Hidmark and M. Fischer and Z.
                      Kender and C. Schwab and I. Hausser and J. Weis and S.
                      Dihlmann and D. Böckler and M. Bendszus and S. Heiland and
                      S. Herzig and P. P. Nawroth and J. Szendroedi and T.
                      Fleming},
      title        = {{E}xploring {S}tructural and {M}olecular {F}eatures of
                      {S}ciatic {N}erve {L}esions in {D}iabetic {N}europathy:
                      {U}nveiling {P}athogenic {P}athways and {T}argets.},
      journal      = {Diabetes},
      volume       = {74},
      number       = {1},
      issn         = {0012-1797},
      address      = {Alexandria, Va},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2024-02091},
      pages        = {65-74},
      year         = {2025},
      note         = {2025 Jan 1;74(1):65-74},
      abstract     = {Lesioned fascicles (LF) in the sciatic nerves of
                      individuals with diabetic neuropathy (DN) correlate with
                      clinical symptom severity. This study aimed to characterize
                      the structural and molecular composition of these lesions to
                      better understand DN pathogenesis. Sciatic nerves from
                      amputees with and without type 2 diabetes (T2D) were
                      examined using ex vivo magnetic resonance neurography, in
                      vitro imaging, and proteomic analysis. Lesions were only
                      found in T2D donors and exhibited significant structural
                      abnormalities, including axonal degeneration, demyelination,
                      and impaired blood nerve barrier (BNB). While non-lesioned
                      fascicles from T2D donors showed activation of
                      neuroprotective pathways, lesioned fascicles lacked this
                      response and instead displayed increased complement
                      activation via the classical pathway. The detection of
                      liver-derived acute-phase proteins suggests that BNB
                      disruption facilitates harmful inter-organ communication
                      between the liver and nerves. These findings reveal key
                      molecular mechanisms contributing to DN and highlight
                      potential targets for therapeutic intervention.},
      cin          = {B350 / HD01 / W120},
      ddc          = {610},
      cid          = {I:(DE-He78)B350-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)W120-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39418320},
      doi          = {10.2337/db24-0493},
      url          = {https://inrepo02.dkfz.de/record/294070},
}