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@ARTICLE{Simats:271707,
      author       = {Simats, Alba and Zhang, Sijia and Messerer, Denise and
                      Chong, Faye and Beşkardeş, Sude and Chivukula, Aparna
                      Sharma and Cao, Jiayu and Besson-Girard, Simon and
                      Montellano, Felipe A and Morbach, Caroline and Carofiglio,
                      Olga and Ricci, Alessio and Roth, Stefan and Llovera, Gemma
                      and Singh, Rashween and Chen, Yiming and Filser, Severin and
                      Plesnila, Nikolaus and Braun, Christian and Spitzer, Hannah
                      and Gokce, Ozgun and Dichgans, Martin and Heuschmann, Peter
                      U and Hatakeyama, Kinta and Beltrán, Eduardo and Clauss,
                      Sebastian and Bonev, Boyan and Schulz, Christian and Liesz,
                      Arthur},
      title        = {{I}nnate immune memory after brain injury drives
                      inflammatory cardiac dysfunction.},
      journal      = {Cell},
      volume       = {187},
      number       = {17},
      issn         = {0092-8674},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2024-01059},
      pages        = {4637 - 4655.e26},
      year         = {2024},
      abstract     = {The medical burden of stroke extends beyond the brain
                      injury itself and is largely determined by chronic
                      comorbidities that develop secondarily. We hypothesized that
                      these comorbidities might share a common immunological
                      cause, yet chronic effects post-stroke on systemic immunity
                      are underexplored. Here, we identify myeloid innate immune
                      memory as a cause of remote organ dysfunction after stroke.
                      Single-cell sequencing revealed persistent pro-inflammatory
                      changes in monocytes/macrophages in multiple organs up to 3
                      months after brain injury, notably in the heart, leading to
                      cardiac fibrosis and dysfunction in both mice and stroke
                      patients. IL-1β was identified as a key driver of
                      epigenetic changes in innate immune memory. These changes
                      could be transplanted to naive mice, inducing cardiac
                      dysfunction. By neutralizing post-stroke IL-1β or blocking
                      pro-inflammatory monocyte trafficking with a CCR2/5
                      inhibitor, we prevented post-stroke cardiac dysfunction.
                      Such immune-targeted therapies could potentially prevent
                      various IL-1β-mediated comorbidities, offering a framework
                      for secondary prevention immunotherapy.},
      keywords     = {Animals / Immunity, Innate / Mice / Interleukin-1beta:
                      metabolism / Brain Injuries: immunology / Humans / Male /
                      Monocytes: metabolism / Monocytes: immunology / Immunologic
                      Memory / Mice, Inbred C57BL / Inflammation: immunology /
                      Macrophages: immunology / Macrophages: metabolism / Stroke:
                      complications / Stroke: immunology / Heart Diseases:
                      immunology / Female / Receptors, CCR2: metabolism / Fibrosis
                      / Epigenesis, Genetic / Trained Immunity / brain ischemia
                      (Other) / cardiac fibrosis (Other) / cenicriviroc (Other) /
                      innate immune memory (Other) / interleukin-1 (Other) /
                      myeloid cells (Other) / stroke (Other) / systemic
                      inflammation (Other) / trained immunity (Other) /
                      Interleukin-1beta (NLM Chemicals) / Receptors, CCR2 (NLM
                      Chemicals)},
      cin          = {AG Dichgans / AG Gokce},
      ddc          = {610},
      cid          = {I:(DE-2719)5000022 / I:(DE-2719)1013041},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 351 -
                      Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39043180},
      doi          = {10.1016/j.cell.2024.06.028},
      url          = {https://pub.dzne.de/record/271707},
}