Clin Res Cardiol (2023). https://doi.org/10.1007/s00392-023-02180-w |
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Clonal hematopoiesis associated TET2 and DNMT3A gene driver mutations accelerates aortic valve calcification in vitro and in vivo | ||
W. Abplanalp1, B. Schuhmacher1, S. Mas-Peiro2, J. Fuster3, M. Shumliakivska4, D. John1, M. Nicotera2, M. Merten1, S. Dimmeler5, A. M. Zeiher6 | ||
1Institute of Cardiovascular Regeneration and Department of Cardiology, Goethe Universität Frankfurt am Main, Frankfurt am Main; 2Med. Klinik III - Kardiologie, Angiologie, Universitätsklinikum Frankfurt, Frankfurt am Main; 3Centro Nacional de Investigaciones Cardiovasculares (CNIC), 28029, ES; 4Zentrum für Molekulare Medizin, Institut für Kardiovaskuläre Regeneration, Universitätsklinikum Frankfurt, Frankfurt am Main; 5Zentrum für Molekulare Medizin, Institut für Kardiovaskuläre Regeneration, Goethe Universität Frankfurt am Main, Frankfurt am Main; 6Institute of Cardiovascular Regeneration, Goethe Universität Frankfurt am Main, Frankfurt am Main; | ||
Calcific
aortic valve disease (CAVD) is the most common age-related heart valve disease,
with no medical therapy to halt progression. Age is associated with the
enrichment of somatic mutations in hematopoietic stem cells leading to clonal
hematopoiesis (CH). CH mutations promote inflammation, occur in > 30% of
patients with severe CAVD and CAVD patients harboring CH mutations have a worse
prognosis. |
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https://dgk.org/kongress_programme/jt2023/aP1362.html |