Home > Publications database > The cellular and molecular cardiac tissue responses in human inflammatory cardiomyopathies after SARS-CoV-2 infection and COVID-19 vaccination. > print |
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024 | 7 | _ | |a 10.1038/s44161-025-00612-6 |2 doi |
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041 | _ | _ | |a English |
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100 | 1 | _ | |a Maatz, Henrike |b 0 |
245 | _ | _ | |a The cellular and molecular cardiac tissue responses in human inflammatory cardiomyopathies after SARS-CoV-2 infection and COVID-19 vaccination. |
260 | _ | _ | |a London |c 2025 |b Nature Publishing Group UK |
336 | 7 | _ | |a article |2 DRIVER |
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336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1743509307_10960 |2 PUB:(DE-HGF) |
336 | 7 | _ | |a ARTICLE |2 BibTeX |
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336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
500 | _ | _ | |a 2025 Mar;4(3):330-345 |
520 | _ | _ | |a Myocarditis, characterized by inflammatory cell infiltration, can have multiple etiologies, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection or, rarely, mRNA-based coronavirus disease 2019 (COVID-19) vaccination. The underlying cellular and molecular mechanisms remain poorly understood. In this study, we performed single-nucleus RNA sequencing on left ventricular endomyocardial biopsies from patients with myocarditis unrelated to COVID-19 (Non-COVID-19), after SARS-CoV-2 infection (Post-COVID-19) and after COVID-19 vaccination (Post-Vaccination). We identified distinct cytokine expression patterns, with interferon-γ playing a key role in Post-COVID-19, and upregulated IL16 and IL18 expression serving as a hallmark of Post-Vaccination myocarditis. Although myeloid responses were similar across all groups, the Post-Vaccination group showed a higher proportion of CD4+ T cells, and the Post-COVID-19 group exhibited an expansion of cytotoxic CD8+ T and natural killer cells. Endothelial cells showed gene expression changes indicative of vascular barrier dysfunction in the Post-COVID-19 group and ongoing angiogenesis across all groups. These findings highlight shared and distinct mechanisms driving myocarditis in patients with and without a history of SARS-CoV-2 infection or vaccination. |
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700 | 1 | _ | |a Lindberg, Eric L |b 1 |
700 | 1 | _ | |a Adami, Eleonora |b 2 |
700 | 1 | _ | |a López-Anguita, Natalia |b 3 |
700 | 1 | _ | |a Perdomo-Sabogal, Alvaro |0 0000-0002-1677-8963 |b 4 |
700 | 1 | _ | |a Cocera Ortega, Lucía |b 5 |
700 | 1 | _ | |a Patone, Giannino |0 0000-0002-7242-0341 |b 6 |
700 | 1 | _ | |a Reichart, Daniel |b 7 |
700 | 1 | _ | |a Myronova, Anna |b 8 |
700 | 1 | _ | |a Schmidt, Sabine |b 9 |
700 | 1 | _ | |a Elsanhoury, Ahmed |b 10 |
700 | 1 | _ | |a Klein, Oliver |b 11 |
700 | 1 | _ | |a Kühl, Uwe |b 12 |
700 | 1 | _ | |a Wyler, Emanuel |0 0000-0002-9884-1806 |b 13 |
700 | 1 | _ | |a Landthaler, Markus |0 0000-0002-1075-8734 |b 14 |
700 | 1 | _ | |a Yousefian, Schayan |b 15 |
700 | 1 | _ | |a Haas, Simon |0 P:(DE-He78)a5ec4e2fef99022a37a6b07c2fdd6325 |b 16 |
700 | 1 | _ | |a Kurth, Florian |0 0000-0002-3807-473X |b 17 |
700 | 1 | _ | |a Teichmann, Sarah A |0 0000-0002-6294-6366 |b 18 |
700 | 1 | _ | |a Oudit, Gavin Y |b 19 |
700 | 1 | _ | |a Milting, Hendrik |b 20 |
700 | 1 | _ | |a Noseda, Michela |0 0000-0002-9553-5029 |b 21 |
700 | 1 | _ | |a Seidman, Jonathan G |0 0000-0002-9082-3566 |b 22 |
700 | 1 | _ | |a Seidman, Christine E |0 0000-0001-6380-1209 |b 23 |
700 | 1 | _ | |a Heidecker, Bettina |b 24 |
700 | 1 | _ | |a Sander, Leif E |0 0000-0002-0476-9947 |b 25 |
700 | 1 | _ | |a Sawitzki, Birgit |0 0000-0001-8166-8579 |b 26 |
700 | 1 | _ | |a Klingel, Karin |b 27 |
700 | 1 | _ | |a Doeblin, Patrick |b 28 |
700 | 1 | _ | |a Kelle, Sebastian |0 0000-0001-8105-6599 |b 29 |
700 | 1 | _ | |a Van Linthout, Sophie |b 30 |
700 | 1 | _ | |a Hubner, Norbert |0 0000-0002-1218-6223 |b 31 |
700 | 1 | _ | |a Tschöpe, Carsten |b 32 |
773 | _ | _ | |a 10.1038/s44161-025-00612-6 |0 PERI:(DE-600)3076837-8 |n 3 |p 330-345 |t Nature cardiovascular research |v 4 |y 2025 |x 2731-0590 |
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