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@ARTICLE{Weber:280916,
      author       = {Weber, Alexander N R and McManus, Róisín M and Hornung,
                      Veit and Geyer, Matthias and Kuemmerle-Deschner, Jasmin B
                      and Latz, Eicke},
      title        = {{T}he expanding role of the {NLRP}3 inflammasome from
                      periodic fevers to therapeutic targets.},
      journal      = {Nature immunology},
      volume       = {26},
      number       = {9},
      issn         = {1529-2908},
      address      = {London},
      publisher    = {Springer Nature Limited},
      reportid     = {DZNE-2025-00999},
      pages        = {1453 - 1466},
      year         = {2025},
      abstract     = {Understanding and treating inflammation has proven a
                      formidable challenge. The initiator and central motor of
                      inflammation, the protein NLRP3, is an innate immune
                      sentinel and nonspecific sensor of cellular perturbation. A
                      wide array of inflammatory triggers prompts the formation of
                      an NLRP3 'inflammasome' complex, leading to inflammatory
                      interleukin-1 family cytokine release and pyroptotic cell
                      death. Since gain-of-function mutations in NLRP3 were
                      demonstrated to cause a rare autoinflammatory disease termed
                      cryopyrin-associated periodic syndrome, NLRP3 has emerged as
                      key mediator of inflammation in mouse models for many common
                      diseases, including atherosclerosis, Alzheimer's disease and
                      gout. But even though small-molecule NLRP3 modulators have
                      entered clinical development, many aspects of NLRP3
                      activation and regulation in humans remain relatively
                      unclear. This Review summarizes the current understanding of
                      the molecular mechanisms that drive NLRP3 inflammasome
                      activation and regulation, and discusses emerging targeting
                      strategies. Understanding these processes can guide
                      precision medicine approaches aimed at mitigating
                      NLRP3-driven pathologies.},
      subtyp        = {Review Article},
      keywords     = {NLR Family, Pyrin Domain-Containing 3 Protein: metabolism /
                      NLR Family, Pyrin Domain-Containing 3 Protein: genetics /
                      NLR Family, Pyrin Domain-Containing 3 Protein: immunology /
                      Humans / Inflammasomes: metabolism / Inflammasomes:
                      immunology / Animals / Cryopyrin-Associated Periodic
                      Syndromes: immunology / Cryopyrin-Associated Periodic
                      Syndromes: drug therapy / Cryopyrin-Associated Periodic
                      Syndromes: genetics / Mice / Inflammation: immunology / NLR
                      Family, Pyrin Domain-Containing 3 Protein (NLM Chemicals) /
                      Inflammasomes (NLM Chemicals) / NLRP3 protein, human (NLM
                      Chemicals)},
      cin          = {AG McManus},
      ddc          = {610},
      cid          = {I:(DE-2719)1013042},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40826276},
      doi          = {10.1038/s41590-025-02230-7},
      url          = {https://pub.dzne.de/record/280916},
}