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@ARTICLE{Furkel:305559,
      author       = {J. Furkel$^*$ and V. A. Zirkenbach and M. Knoll$^*$ and R.
                      Öttl and K. Rein$^*$ and A. Abdollahi$^*$ and N. Frey and
                      M. H. Konstandin and Z. Kaya},
      title        = {{C}ardiac {T}roponin {I} {A}ntibodies {I}nduce
                      {C}ardiomyocyte {D}amage and {A}lter {C}ell {M}orphology.},
      journal      = {International journal of molecular sciences},
      volume       = {26},
      number       = {20},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DKFZ-2025-02229},
      pages        = {10005},
      year         = {2025},
      note         = {#EA:E210#},
      abstract     = {Circulating heart-reactive autoantibodies (aAbs) detected
                      in a variety of heart diseases (e.g., myocarditis, dilated
                      cardiomyopathy, and myocardial infarction) have been
                      associated with the progression of heart failure and a poor
                      prognosis. However, the underlying mechanisms remain largely
                      unknown. We investigated the effects of murine plasma
                      containing aAbs against cardiac troponin I (cTnI) on
                      neonatal rat cardiomyocytes (NRCMs). An autoimmune response
                      to cTnI in A/J mice was induced, and anti-cTnI-aAbs were
                      quantified. After 21 days, cardiac function, inflammation,
                      fibrosis, and apoptosis were evaluated. In complementary in
                      vitro liquid biopsy experiments, NRCMs were incubated with
                      murine plasma containing high anti-cTnI-aAb levels or
                      corresponding controls. Morphological phenotyping was
                      performed using the C-MORE fluorescent image-based analysis
                      workflow. Immunization with cTnI resulted in high
                      anti-cTnI-aAb production, followed by myocardial
                      inflammation, fibrosis, and impaired ejection fraction.
                      NRCMs exposed to anti-cTnI-aAb-containing plasma showed
                      reduced cell size, altered shape and radius, and elevated
                      rate of dead cells in cell cycle analysis (p < 0.01, for
                      $20\%$ plasma). Together, these findings suggest a direct
                      interaction of anti-cTnI-aAbs on cardiomyocytes, likely
                      promoting adverse myocardial remodeling in vivo.},
      keywords     = {Animals / Myocytes, Cardiac: pathology / Myocytes, Cardiac:
                      immunology / Myocytes, Cardiac: metabolism / Troponin I:
                      immunology / Autoantibodies: immunology / Autoantibodies:
                      blood / Rats / Mice / Fibrosis / Apoptosis / Animals,
                      Newborn / Male / autoantibodies (Other) / cardiomyocytes
                      (Other) / heart failure (Other) / morphology (Other) /
                      troponin I (Other) / Troponin I (NLM Chemicals) /
                      Autoantibodies (NLM Chemicals)},
      cin          = {E210 / HD01},
      ddc          = {540},
      cid          = {I:(DE-He78)E210-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {315 - Bildgebung und Radioonkologie (POF4-315)},
      pid          = {G:(DE-HGF)POF4-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41155300},
      doi          = {10.3390/ijms262010005},
      url          = {https://inrepo02.dkfz.de/record/305559},
}