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@ARTICLE{Mueller:291568,
      author       = {K. A. L. Mueller and C. Langnau and T. Harm and M. Sigle
                      and K. Mott and M. Droppa and O. Borst and A.-K. Rohlfing
                      and S. Gekeler and M. Günter$^*$ and N. Goebel and U. F. W.
                      Franke and M. Radwan and C. Schlensak and H. Janning and S.
                      Scheuermann and C. M. Seitz and D. Rath and K.-P.
                      Kreisselmeier and T. Castor and I. I. Mueller and H. Schulze
                      and S. Autenrieth$^*$ and M. P. Gawaz},
      title        = {{M}acrophage {M}igration {I}nhibitory {F}actor {P}romotes
                      {T}hromboinflammation and {P}redicts {F}ast {P}rogression of
                      {A}ortic {S}tenosis.},
      journal      = {Arteriosclerosis, thrombosis, and vascular biology},
      volume       = {44},
      number       = {9},
      issn         = {0276-5047},
      address      = {Stanford, Calif.},
      publisher    = {HighWire},
      reportid     = {DKFZ-2024-01453},
      pages        = {2118-2135},
      year         = {2024},
      note         = {#LA:D431# / 2024 Sep;44(9):2118-2135},
      abstract     = {Aortic stenosis (AS) is driven by progressive inflammatory
                      and fibrocalcific processes regulated by circulating
                      inflammatory and valve resident endothelial and interstitial
                      cells. The impact of platelets, platelet-derived mediators,
                      and platelet-monocyte interactions on the acceleration of
                      local valvular inflammation and mineralization is presently
                      unknown.We prospectively enrolled 475 consecutive patients
                      with severe symptomatic AS undergoing aortic valve
                      replacement. Clinical workup included repetitive
                      echocardiography, analysis of platelets, monocytes,
                      chemokine profiling, aortic valve tissue samples for
                      immunohistochemistry, and gene expression analysis.The
                      patients were classified as fast-progressive AS by the
                      median ∆Vmax of 0.45 m/s per year determined by
                      echocardiography. Immunohistological aortic valve analysis
                      revealed enhanced cellularity in fast-progressive AS (slow-
                      versus fast-progressive AS; median [interquartile range],
                      247 [142.3-504] versus 717.5 [360.5-1234]; P<0.001) with
                      less calcification (calcification area, mm2: 33.74
                      [27.82-41.86] versus 20.54 [13.52-33.41]; P<0.001). MIF
                      (macrophage migration inhibitory factor)-associated gene
                      expression was significantly enhanced in fast-progressive AS
                      accompanied by significantly elevated MIF plasma levels
                      (mean±SEM; 6877±379.1 versus 9959±749.1; P<0.001),
                      increased platelet activation, and decreased intracellular
                      MIF expression indicating enhanced MIF release upon platelet
                      activation (CD62P, $\%:$ median [interquartile range], 16.8
                      [11.58-23.8] versus 20.55 [12.48-32.28], P=0.005; MIF, $\%:$
                      4.85 [1.48-9.75] versus 2.3 [0.78-5.9], P<0.001). Regression
                      analysis confirmed that MIF-associated biomarkers are
                      strongly associated with an accelerated course of AS.Our
                      findings suggest a key role for platelet-derived MIF and its
                      interplay with circulating and valve resident
                      monocytes/macrophages in local and systemic
                      thromboinflammation during accelerated AS. MIF-based
                      biomarkers predict an accelerated course of AS and represent
                      a novel pharmacological target to attenuate progression of
                      AS.},
      keywords     = {aortic valve stenosis (Other) / biomarkers (Other) / blood
                      platelets (Other) / chemokines (Other) / inflammation
                      (Other)},
      cin          = {D431},
      ddc          = {610},
      cid          = {I:(DE-He78)D431-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38989580},
      doi          = {10.1161/ATVBAHA.124.321000},
      url          = {https://inrepo02.dkfz.de/record/291568},
}