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@ARTICLE{Hew:282300,
      author       = {Hew, Lois and Maierhof, Smilla K and Ivanov, Andranik and
                      Beule, Dieter and Fernandez Vallone, Valeria and
                      Stachelscheid, Harald and Frahm, Silke and Telugu, Narasimha
                      Swamy and Endres, Matthias and Boehmerle, Wolfgang and
                      Huehnchen, Petra and Schinke, Christian},
      title        = {c-{J}un inhibition mitigates chemotherapy-induced
                      neurotoxicity in i{PSC}-derived sensory neurons.},
      journal      = {Cell death discovery},
      volume       = {11},
      number       = {1},
      issn         = {2058-7716},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DZNE-2025-01270},
      pages        = {529},
      year         = {2025},
      abstract     = {Chemotherapy-induced peripheral neuropathy (CIPN) affects
                      up to two-thirds of cancer patients undergoing cytotoxic
                      chemotherapy. Here, we used human iPSC-derived sensory
                      neurons (iPSC-DSN) to model CIPN in vitro. Administration of
                      various chemotherapeutic agents (i.e., paclitaxel,
                      vincristine, bortezomib and cisplatin) at clinically
                      applicable concentrations resulted in reduced cell
                      viability, axonal degeneration, electrophysiological
                      dysfunction and increased levels of phosphorylated c-Jun in
                      iPSC-DSN. Transcriptomic analyses revealed that the
                      upregulation of c-Jun strongly correlated with the
                      expression of genes of neuronal injury, apoptosis and
                      inflammatory signatures. To test whether c-Jun plays a
                      central role in the development of CIPN, we applied the
                      small molecule inhibitor of the Jun N-terminal kinase,
                      SP600125, to iPSC-DSN treated with neurotoxic chemotherapy.
                      c-Jun inhibition prevented chemotherapy-induced
                      neurotoxicity by preserving cell viability, axonal integrity
                      and electrophysiological function of iPSC-DSN. These
                      findings identify c-Jun as a key mediator of CIPN
                      pathophysiology across multiple drug types and present
                      preclinical evidence that c-Jun inhibition is an attractive
                      therapeutic target to prevent CIPN.},
      cin          = {AG Endres},
      ddc          = {610},
      cid          = {I:(DE-2719)1811005},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41233356},
      pmc          = {pmc:PMC12615653},
      doi          = {10.1038/s41420-025-02847-5},
      url          = {https://pub.dzne.de/record/282300},
}