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@ARTICLE{Tonnus:303496,
      author       = {W. Tonnus and F. Maremonti and S. Gavali and M. N. Schlecht
                      and F. Gembardt and A. Belavgeni and N. Leinung and K. Flade
                      and N. Bethe and S. Traikov and A. Haag and D. Schilling$^*$
                      and S. Penkov and M. Mallais and C. Gaillet and C. Meyer and
                      M. Katebi and A. Ray and L. M. S. Gerhardt and A. Brucker
                      and J. N. Becker and M. Tmava and L. Schlicker$^*$ and A.
                      Schulze$^*$ and N. Himmerkus and A. Shevchenko and M.
                      Peitzsch and U. Barayeu and S. Nasi and J. Putz and K. S.
                      Korach and J. Neugarten and L. Golestaneh and C. Hugo and J.
                      U. Becker and J. M. Weinberg and S. Lorenz and B. Proneth
                      and M. Conrad and E. Wolf and B. Plietker and R. Rodriguez
                      and D. A. Pratt and T. P. Dick$^*$ and M. Fedorova and S. R.
                      Bornstein and A. Linkermann},
      title        = {{M}ultiple oestradiol functions inhibit ferroptosis and
                      acute kidney injury.},
      journal      = {Nature},
      volume       = {nn},
      issn         = {0028-0836},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2025-01687},
      pages        = {nn},
      year         = {2025},
      note         = {DKFZ-ZMBH Alliance / epub},
      abstract     = {Acute tubular necrosis mediates acute kidney injury (AKI)
                      and nephron loss1, the hallmark of end-stage renal
                      disease2-4. For decades, it has been known that female
                      kidneys are less sensitive to AKI5,6. Acute tubular necrosis
                      involves dynamic cell death propagation by ferroptosis along
                      the tubular compartment7,8. Here we demonstrate abrogated
                      ferroptotic cell death propagation in female kidney tubules.
                      17β-oestradiol establishes an anti-ferroptotic state
                      through non-genomic and genomic mechanisms. These include
                      the potent direct inhibition of ferroptosis by
                      hydroxyoestradiol derivatives, which function as radical
                      trapping antioxidants, are present at high concentrations in
                      kidney tubules and, when exogenously applied, protect male
                      mice from AKI. In cells, the oxidized hydroxyoestradiols are
                      recycled by FSP19,10, but FSP1-deficient female mice were
                      not sensitive to AKI. At the genomic level, female
                      ESR1-deficient kidney tubules partially lose their
                      anti-ferroptotic capacity, similar to ovariectomized mice.
                      While ESR1 promotes the anti-ferroptotic hydropersulfide
                      system, male tubules express pro-ferroptotic proteins of the
                      ether lipid pathway which are suppressed by ESR1 in female
                      tissues until menopause. In summary, we identified
                      non-genomic and genomic mechanisms that collectively explain
                      ferroptosis resistance in female tubules and may function as
                      therapeutic targets for male and postmenopausal female
                      individuals.},
      cin          = {A160 / A410},
      ddc          = {500},
      cid          = {I:(DE-He78)A160-20160331 / 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:40804518},
      doi          = {10.1038/s41586-025-09389-x},
      url          = {https://inrepo02.dkfz.de/record/303496},
}