The S protein of SARS-CoV-2 injures cardiomyocytes indirectly through the release of cytokines instead of direct action

Wei Ting Chang, Yu Wen Lin, Zhih Cherng Chen, Ping Yen Liu

研究成果: Article同行評審

1 引文 斯高帕斯(Scopus)

摘要

Background: Emerging evidence has shown that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with cardiac injury, but it remains unclear whether cardiac injury is mainly caused by direct viral infection or is secondary to SARS-CoV-2-induced cytokine storm. Methods: Through directly treating cardiomyocytes with S protein, a crucial surface protein of SARS-CoV-2, and indirectly treating cardiomyocytes with S protein-derived human T lymphocyte conditioned medium, we compared the intensities of cardiomyocyte injuries caused by either S protein of the virus or S protein of virus-triggered cytokines. Results: The directly treated cardiomyocytes did not show increasing cell apoptosis. In contrast, cardiomyocytes treated with the supernatant medium of S protein pre-conditioned peripheral blood mononuclear cells showed significantly suppressed viability. In addition, using a cardiovascular disease-specific PCR array, genes associated with hypertrophy, apoptosis, inflammation and angiogenesis were observed to be affected by cytokine stress. Conclusions: Collectively, we found that SARS-CoV-2-induced heart injury may be mainly through the S protein of the virus enhancing host immune responses instead of the S protein of the virus per se. With regards to clinical application, the strategy for treating COVID-19 should not only focus on anti-viral therapy but also on suppressing over-activated immunity.

原文English
頁(從 - 到)643-647
頁數5
期刊Acta Cardiologica Sinica
37
發行號6
DOIs
出版狀態Published - 2021 11月

All Science Journal Classification (ASJC) codes

  • 心臟病學與心血管醫學

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