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@ARTICLE{Yapici:300702,
      author       = {F. I. Yapici and E. Seidel and A. Dahlhaus and J. Weber and
                      C. Schmidt and A. de Britto Chaves Filho$^*$ and M. Yang and
                      M. Nenchova and E. Güngör and J. Stroh and I. Kotouza and
                      J. Beck and A. T. Abdallah and J.-W. Lackmann and C. M.
                      Bebber and A. Androulidaki and P. Kreuzaler and A.
                      Schulze$^*$ and C. Frezza and S. von Karstedt},
      title        = {{A}n atlas of ferroptosis-induced secretomes.},
      journal      = {Cell death and differentiation},
      volume       = {nn},
      issn         = {1350-9047},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-00882},
      pages        = {nn},
      year         = {2025},
      note         = {epub / DKFZ-ZMBH Alliance},
      abstract     = {Cells undergoing regulated necrosis systemically
                      communicate with the immune system via the release of
                      protein and non-protein secretomes. Ferroptosis is a
                      recently described iron-dependent type of regulated necrosis
                      driven by massive lipid peroxidation. While membrane rupture
                      occurs during ferroptosis, a comprehensive appraisal of
                      ferroptotic secretomes and their potential biological
                      activity has been lacking. Here, we apply a multi-omics
                      approach to provide an atlas of ferroptosis-induced
                      secretomes and reveal a novel function in macrophage
                      priming. Proteins with assigned DAMP and innate immune
                      system function, such as MIF, heat shock proteins (HSPs),
                      and chaperones, were released from ferroptotic cells.
                      Non-protein secretomes with assigned inflammatory function
                      contained oxylipins as well as TCA- and methionine-cycle
                      metabolites. Interestingly, incubation of bone
                      marrow-derived macrophages (BMDMs) with ferroptotic
                      supernatants induced transcriptional reprogramming
                      consistent with priming. Indeed, exposure to ferroptotic
                      supernatants enhanced LPS-induced cytokine production. These
                      results define a catalog of ferroptosis-induced secretomes
                      and identify a biological activity in macrophage priming
                      with important implications for the fine-tuning of
                      inflammatory processes.},
      cin          = {A410},
      ddc          = {610},
      cid          = {I:(DE-He78)A410-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40281125},
      doi          = {10.1038/s41418-025-01517-4},
      url          = {https://inrepo02.dkfz.de/record/300702},
}