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@ARTICLE{Saller:275933,
      author       = {Saller, Benedikt S and Wöhrle, Svenja and Fischer, Larissa
                      and Dufossez, Clara and Ingerl, Isabella L and Kessler,
                      Susanne and Mateo-Tortola, Maria and Gorka, Oliver and
                      Lange, Felix and Cheng, Yurong and Neuwirt, Emilia and
                      Marada, Adinarayana and Koentges, Christoph and Urban,
                      Chiara and Aktories, Philipp and Reuther, Peter and Giese,
                      Sebastian and Kirschnek, Susanne and Mayer, Carolin and
                      Pilic, Johannes and Falquez-Medina, Hugo and Oelgeklaus,
                      Aline and Deepagan, Veerasikku Gopal and Shojaee, Farzaneh
                      and Zimmermann, Julia A and Weber, Damian and Tai, Yi-Heng
                      and Crois, Anna and Ciminski, Kevin and Peyronnet, Remi and
                      Brandenburg, Katharina S and Wu, Gang and Baumeister, Ralf
                      and Heimbucher, Thomas and Rizzi, Marta and Riedel, Dietmar
                      and Helmstädter, Martin and Buescher, Joerg and Neumann,
                      Konstantin and Misgeld, Thomas and Kerschensteiner, Martin
                      and Walentek, Peter and Kreutz, Clemens and Maurer, Ulrich
                      and Rambold, Angelika S and Vince, James E and Edlich, Frank
                      and Malli, Roland and Häcker, Georg and Kierdorf, Katrin
                      and Meisinger, Chris and Köttgen, Anna and Jakobs, Stefan
                      and Weber, Alexander N R and Schwemmle, Martin and Groß,
                      Christina J and Groß, Olaf},
      title        = {{A}cute suppression of mitochondrial {ATP} production
                      prevents apoptosis and provides an essential signal for
                      {NLRP}3 inflammasome activation.},
      journal      = {Immunity},
      volume       = {58},
      number       = {1},
      issn         = {1074-7613},
      address      = {[Cambridge, Mass.]},
      publisher    = {Cell Press},
      reportid     = {DZNE-2025-00155},
      pages        = {90 - 107.e11},
      year         = {2025},
      abstract     = {How mitochondria reconcile roles in functionally divergent
                      cell death pathways of apoptosis and NLRP3
                      inflammasome-mediated pyroptosis remains elusive, as is
                      their precise role in NLRP3 activation and the
                      evolutionarily conserved physiological function of NLRP3.
                      Here, we have shown that when cells were challenged
                      simultaneously, apoptosis was inhibited and NLRP3 activation
                      prevailed. Apoptosis inhibition by structurally diverse
                      NLRP3 activators, including nigericin, imiquimod,
                      extracellular ATP, particles, and viruses, was not a
                      consequence of inflammasome activation but rather of their
                      effects on mitochondria. NLRP3 activators turned out as
                      oxidative phosphorylation (OXPHOS) inhibitors, which we
                      found to disrupt mitochondrial cristae architecture, leading
                      to trapping of cytochrome c. Although this effect was alone
                      not sufficient for NLRP3 activation, OXPHOS inhibitors
                      became triggers of NLRP3 when combined with resiquimod or
                      Yoda-1, suggesting that NLRP3 activation requires two
                      simultaneous cellular signals, one of mitochondrial origin.
                      Therefore, OXPHOS and apoptosis inhibition by NLRP3
                      activators provide stringency in cell death decisions.},
      keywords     = {NLR Family, Pyrin Domain-Containing 3 Protein: metabolism /
                      Inflammasomes: metabolism / Mitochondria: metabolism /
                      Apoptosis / Adenosine Triphosphate: metabolism / Animals /
                      Mice / Oxidative Phosphorylation / Humans / Signal
                      Transduction / Mice, Inbred C57BL / Pyroptosis / ATP (Other)
                      / NLRP3 (Other) / OXPHOS (Other) / apoptosis (Other) /
                      bioenergetics (Other) / cell death (Other) / chemical
                      biology (Other) / cytochrome c (Other) / inflammasome
                      (Other) / mitochondria (Other) / pyroptosis (Other) / NLR
                      Family, Pyrin Domain-Containing 3 Protein (NLM Chemicals) /
                      Inflammasomes (NLM Chemicals) / Adenosine Triphosphate (NLM
                      Chemicals) / Nlrp3 protein, mouse (NLM Chemicals)},
      cin          = {AG Misgeld},
      ddc          = {610},
      cid          = {I:(DE-2719)1110000-4},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39571574},
      doi          = {10.1016/j.immuni.2024.10.012},
      url          = {https://pub.dzne.de/record/275933},
}