Tangos, Melina and Budde, Heidi and Kolijn, Detmar and Sieme, Marcel and Zhazykbayeva, Saltanat and Lodi, Maria and Herwig, Melissa and Goemoeri, Kamilla and Hassoun, Roua and Robinson, Emma Louise and Meister, Toni Luise and Jaquet, Kornelia and Kovacs, Arpad and Mustroph, Julian and Evert, Katja and Babel, Nina and Fagyas, Miklos and Lindner, Diana and Pueschel, Klaus and Westermann, Dirk and Mannherz, Hans Georg and Paneni, Francesco and Pfaender, Stephanie and Toth, Attila and Mugge, Andreas and Sossalla, Samuel and Hamdani, Nazha (2022) SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress. INTERNATIONAL JOURNAL OF CARDIOLOGY, 362. pp. 196-205. ISSN 0167-5273, 1874-1754
Full text not available from this repository. (Request a copy)Abstract
Introduction: The respiratory illness triggered by severe acute respiratory syndrome virus-2 (SARS-CoV-2) is often particularly serious or fatal amongst patients with pre-existing heart conditions. Although the mechanisms underlying SARS-CoV-2-related cardiac damage remain elusive, inflammation (i.e. 'cytokine storm') and oxidative stress are likely involved. Methods and results: Here we sought to determine: 1) if cardiomyocytes are targeted by SARS-CoV-2 and 2) how inflammation and oxidative stress promote the viral entry into cardiac cells. We analysed pro-inflammatory and oxidative stress and its impact on virus entry and virus-associated cardiac damage from SARS-CoV-2 infected patients and compared it to left ventricular myocardial tissues obtained from non-infected transplanted hearts either from end stage heart failure or non-failing hearts (donor group). We found that neuropilin-1 potentiates SARS-CoV-2 entry into human cardiomyocytes, a phenomenon driven by inflammatory and oxidant signals. These changes accounted for increased pmteases activity and apoptotic markers thus leading to cell damage and apoptosis. Conclusion: This study provides new insights into the mechanisms of SARS-CoV-2 entry into the heart and defines promising targets for antiviral interventions for COVID-19 patients with pre-existing heart conditions or patients with co-morbidities.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | RESPIRATORY SYNDROME CORONAVIRUS; CELL ENTRY; HEART-FAILURE; CATHEPSIN-L; ACTIVATION; PROTEIN; NEUTROPHILS; COVID-19; SARS; SARS-CoV-2; Cardiomyocytes; Inflammation; Oxidative stress; Heart damage |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II Medicine > Lehrstuhl für Pathologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 26 Jan 2024 14:08 |
| Last Modified: | 29 Jan 2024 13:23 |
| URI: | https://pred.uni-regensburg.de/id/eprint/58266 |
Actions (login required)
 |
View Item |
