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@ARTICLE{Asare:277527,
      author       = {Asare, Yaw and Yan, Guangyao and Schlegl, Christina and
                      Prestel, Matthias and van der Vorst, Emiel P C and
                      Teunissen, Abraham J P and Aronova, Arailym and Tosato,
                      Federica and Naser, Nawraa and Caputo, Julio and Prevot,
                      Geoffrey and Azzun, Anthony and Wefers, Benedikt and Wurst,
                      Wolfgang and Schneider, Melanie and Forne, Ignasi and
                      Bidzhekov, Kiril and Naumann, Ronald and van der Laan,
                      Sander W and Brandhofer, Markus and Cao, Jiayu and Roth,
                      Stefan and Malik, Rainer and Tiedt, Steffen and Mulder,
                      Willem J M and Imhof, Axel and Liesz, Arthur and Weber,
                      Christian and Bernhagen, Jürgen and Dichgans, Martin},
      title        = {{A} cis-regulatory element controls expression of histone
                      deacetylase 9 to fine-tune inflammasome-dependent chronic
                      inflammation in atherosclerosis.},
      journal      = {Immunity},
      volume       = {58},
      number       = {3},
      issn         = {1074-7613},
      address      = {[Cambridge, Mass.]},
      publisher    = {Cell Press},
      reportid     = {DZNE-2025-00423},
      pages        = {555 - 567.e9},
      year         = {2025},
      abstract     = {Common genetic variants in a conserved cis-regulatory
                      element (CRE) at histone deacetylase (HDAC)9 are a major
                      risk factor for cardiovascular disease, including stroke and
                      coronary artery disease. Given the consistency of this
                      association and its proinflammatory properties, we examined
                      the mechanisms whereby HDAC9 regulates vascular
                      inflammation. HDAC9 bound and mediated deacetylation of
                      NLRP3 in the NACHT and LRR domains leading to inflammasome
                      activation and lytic cell death. Targeted deletion of the
                      critical CRE in mice increased Hdac9 expression in myeloid
                      cells to exacerbate inflammasome-dependent chronic
                      inflammation. In human carotid endarterectomy samples,
                      increased HDAC9 expression was associated with
                      atheroprogression and clinical plaque instability.
                      Incorporation of TMP195, a class IIa HDAC inhibitor, into
                      lipoprotein-based nanoparticles to target HDAC9 at the site
                      of myeloid-driven vascular inflammation stabilized
                      atherosclerotic plaques, implying a lower risk of plaque
                      rupture and cardiovascular events. Our findings link HDAC9
                      to atherogenic inflammation and provide a paradigm for
                      anti-inflammatory therapeutics for atherosclerosis.},
      keywords     = {Animals / Atherosclerosis: genetics / Atherosclerosis:
                      metabolism / Atherosclerosis: immunology / Histone
                      Deacetylases: metabolism / Histone Deacetylases: genetics /
                      Inflammasomes: metabolism / Humans / Mice / Inflammation:
                      genetics / NLR Family, Pyrin Domain-Containing 3 Protein:
                      metabolism / NLR Family, Pyrin Domain-Containing 3 Protein:
                      genetics / Repressor Proteins: metabolism / Repressor
                      Proteins: genetics / Mice, Knockout / Regulatory Sequences,
                      Nucleic Acid: genetics / Mice, Inbred C57BL / Plaque,
                      Atherosclerotic: metabolism / Plaque, Atherosclerotic:
                      genetics / Gene Expression Regulation / GWAS (Other) / HDAC9
                      (Other) / NLRP3 (Other) / atherosclerosis (Other) /
                      cis-regulatory element (Other) / inflammasome (Other) /
                      inflammation (Other) / nanobiologics (Other) / stroke
                      (Other) / therapeutics (Other) / Histone Deacetylases (NLM
                      Chemicals) / Inflammasomes (NLM Chemicals) / NLR Family,
                      Pyrin Domain-Containing 3 Protein (NLM Chemicals) / HDAC9
                      protein, human (NLM Chemicals) / Hdac9 protein, mouse (NLM
                      Chemicals) / Repressor Proteins (NLM Chemicals)},
      cin          = {AG Dichgans / AG Wurst},
      ddc          = {610},
      cid          = {I:(DE-2719)5000022 / I:(DE-2719)1140001},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39879983},
      doi          = {10.1016/j.immuni.2025.01.003},
      url          = {https://pub.dzne.de/record/277527},
}