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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
New laboratory evidence for the association between endothelial dysfunction and COVID-19 disease progression
Nan Liu1,2, Hui Long3, Jianhua Sun1,2
1School of Pharmacy, University of Chinese Academy of Sciences, Beijing, China.
Insights
This study links male sex, older age, and chronic diseases to poor COVID-19 outcomes. Endothelial dysfunction markers like VCAM-1 and tPA were elevated in COVID-19 patients, suggesting a therapeutic target.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Pathology
Background:
- Endothelial dysfunction is implicated in COVID-19 pathogenesis, but direct laboratory evidence is limited.
- Angiotensin-converting enzyme 2 (ACE2) is expressed on endothelial cells, highlighting the endothelium's role in COVID-19.
- Understanding the link between endothelial dysfunction and COVID-19 prognosis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the association between endothelial dysfunction and clinical prognosis in COVID-19 patients.
- To identify specific endothelial function parameters altered in COVID-19.
- To explore correlations between endothelial dysfunction markers and clinical indicators of disease severity.
Main Methods:
- A multicenter retrospective cohort study of 966 COVID-19 patients was conducted.
- A cross-sectional study compared endothelial function parameters in 39 COVID-19 patients and 41 non-COVID-19 controls.
- Plasma levels of vascular cell adhesion molecule-1 (VCAM-1), E-selectin, tissue-type plasminogen activator (tPA), and plasminogen activator inhibitor-1 were measured.
Main Results:
- Male sex, older age, and comorbidities were associated with poor COVID-19 prognosis.
- COVID-19 patients showed significantly elevated VCAM-1, E-selectin, and tPA, and decreased plasminogen activator inhibitor-1 compared to controls.
- VCAM-1 and tPA positively correlated with d-dimer and blood urea nitrogen, indicating links to coagulation and kidney dysfunction.
Conclusions:
- Endothelial dysfunction is strongly associated with poor prognosis in COVID-19.
- Elevated VCAM-1, E-selectin, tPA, and reduced plasminogen activator inhibitor-1 are key indicators of endothelial dysfunction in COVID-19.
- Targeting endothelial dysfunction presents a promising therapeutic strategy for managing COVID-19.
Abstract:
There is growing evidence that angiotensin-converting enzyme 2 is highly expressed on endothelial cells, endothelial dysfunction plays a critical role in coronavirus disease 2019 (COVID-19) progression, but laboratory evidence is still lacking. This study established a multicenter retrospective cohort of 966 COVID-19 patients from three hospitals in Wuhan, China. We found that male (62.8% vs. 46.5%), old age [72 (17) vs. 60.5 (21)], and coexisting chronic diseases (88.5% vs. 60.0%) were associated with poor clinical prognosis in COVID-19. Furthermore, the deteriorated patients exhibited more severe multiorgan damage, coagulation dysfunction, and extensive inflammation. Additionally, a cross-sectional study including 41 non-COVID-19 controls and 39 COVID-19 patients assayed endothelial function parameters in plasma and showed that COVID-19 patients exhibited elevated vascular cell adhesion molecule-1 (VCAM-1) (median [IQR]: 0.32 [0.27] vs. 0.17 [0.11] μg/ml, p < 0.001), E-selectin (21.06 [12.60] vs. 11.01 [4.63] ng/ml, p < 0.001), tissue-type plasminogen activator (tPA) (0.22 [0.12] vs. 0.09 [0.04] ng/ml, p < 0.001), and decreased plasminogen activator inhibitor-1 (0.75 [1.31] vs 6.20 [5.34] ng/ml, p < 0.001), as compared to normal controls. Moreover, VCAM-1 was positively correlated with d-dimer (R = 0.544, p < 0.001); tPA was positively correlated with d-dimer (R = 0.800, p < 0.001) and blood urea nitrogen (R = 0.638, p < 0.001). Our findings further confirm the strong association between endothelial dysfunction and poor prognosis of COVID-19, which offers a rationale for targeting endothelial dysfunction as a therapeutic strategy for COVID-19.
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