SARS-CoV-2 infection of human iPSC-derived cardiac cells predicts novel cytopathic features in hearts of COVID-19 patients
ABSTRACT Although COVID-19 causes cardiac dysfunction in up to 25% of patients, its pathogenesis remains unclear. Exposure of human iPSC-derived heart cells to SARS-CoV-2 revealed productive infection and robust transcriptomic and morphological signatures of damage, particularly in cardiomyocytes. Transcriptomic disruption of structural proteins corroborated adverse morphologic features, which included a distinct pattern of myofibrillar fragmentation and numerous iPSC-cardiomyocytes lacking nuclear DNA. Human autopsy specimens from COVID-19 patients displayed similar sarcomeric disruption, as well as cardiomyocytes without DNA staining. These striking cytopathic features provide new insights into SARS-CoV-2 induced cardiac damage, offer a platform for discovery of potential therapeutics, and raise serious concerns about the long-term consequences of COVID-19..
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Preprint| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
bioRxiv.org - (2021) vom: 15. Dez. Zur Gesamtaufnahme - year:2021 |
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| Sprache: |
Englisch |
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| Beteiligte Personen: |
Pérez-Bermejo, Juan A. [VerfasserIn] |
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| Links: |
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| doi: |
10.1101/2020.08.25.265561 |
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| PPN (Katalog-ID): |
XBI018633781 |
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| 245 | 1 | 0 | |a SARS-CoV-2 infection of human iPSC-derived cardiac cells predicts novel cytopathic features in hearts of COVID-19 patients |
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| 520 | |a ABSTRACT Although COVID-19 causes cardiac dysfunction in up to 25% of patients, its pathogenesis remains unclear. Exposure of human iPSC-derived heart cells to SARS-CoV-2 revealed productive infection and robust transcriptomic and morphological signatures of damage, particularly in cardiomyocytes. Transcriptomic disruption of structural proteins corroborated adverse morphologic features, which included a distinct pattern of myofibrillar fragmentation and numerous iPSC-cardiomyocytes lacking nuclear DNA. Human autopsy specimens from COVID-19 patients displayed similar sarcomeric disruption, as well as cardiomyocytes without DNA staining. These striking cytopathic features provide new insights into SARS-CoV-2 induced cardiac damage, offer a platform for discovery of potential therapeutics, and raise serious concerns about the long-term consequences of COVID-19. | ||
| 700 | 1 | |a Kang, Serah |e verfasserin |4 aut | |
| 700 | 1 | |a Rockwood, Sarah J. |e verfasserin |4 aut | |
| 700 | 1 | |a Simoneau, Camille R. |e verfasserin |4 aut | |
| 700 | 1 | |a Joy, David A. |e verfasserin |4 aut | |
| 700 | 1 | |a Ramadoss, Gokul N. |e verfasserin |4 aut | |
| 700 | 1 | |a Silva, Ana C. |e verfasserin |4 aut | |
| 700 | 1 | |a Flanigan, Will R. |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Huihui |e verfasserin |4 aut | |
| 700 | 1 | |a Nakamura, Ken |e verfasserin |4 aut | |
| 700 | 1 | |a Whitman, Jeffrey D. |e verfasserin |4 aut | |
| 700 | 1 | |a Ott, Melanie |e verfasserin |4 aut | |
| 700 | 1 | |a Conklin, Bruce R. |e verfasserin |4 aut | |
| 700 | 1 | |a McDevitt, Todd C. |e verfasserin |4 aut | |
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