Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/ijms22105131
Keywords
SARS-CoV-2; endothelial function; thromboinflammation; angiotensin-converting enzyme 2
Funding
- Ministry of Education, Culture, Sports, Science and Technology [18590815, 21590898, 16K19408, 19K17565]
- Japanese Arteriosclerosis Prevention Fund
- Grants-in-Aid for Scientific Research [16K19408, 19K17565] Funding Source: KAKEN
Ask authors/readers for more resources
COVID-19 caused by SARS-CoV-2 poses a worldwide challenge to healthcare systems, with thromboembolism being a major complication contributing to high morbidity and mortality in severe cases. Studies suggest that the direct infection of endothelial cells by SARS-CoV-2 may lead to endothelial dysfunction, resulting in thrombotic complications and severe outcomes in COVID-19 patients.
The outbreak of coronavirus disease 2019 (COVID-19) caused by the betacoronavirus SARS-CoV-2 is now a worldwide challenge for healthcare systems. Although the leading cause of mortality in patients with COVID-19 is hypoxic respiratory failure due to viral pneumonia and acute respiratory distress syndrome, accumulating evidence has shown that the risk of thromboembolism is substantially high in patients with severe COVID-19 and that a thromboembolic event is another major complication contributing to the high morbidity and mortality in patients with COVID-19. Endothelial dysfunction is emerging as one of the main contributors to the pathogenesis of thromboembolic events in COVID-19. Endothelial dysfunction is usually referred to as reduced nitric oxide bioavailability. However, failures of the endothelium to control coagulation, inflammation, or permeability are also instances of endothelial dysfunction. Recent studies have indicated the possibility that SARS-CoV-2 can directly infect endothelial cells via the angiotensin-converting enzyme 2 pathway and that endothelial dysfunction caused by direct virus infection of endothelial cells may contribute to thrombotic complications and severe disease outcomes in patients with COVID-19. In this review, we summarize the current understanding of relationships between SARS-CoV-2 infection, endothelial dysfunction, and pulmonary and extrapulmonary complications in patients with COVID-19.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available