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Updated: Oct 16, 2025
Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
Endothelial dysfunction and COVID-19 (Review)
1Department of Biology, Faculty of Arts and Sciences, University of Balamand, Tripoli PO Box 100, Lebanon.
Insights
Hypertension and cardiovascular disease worsen COVID-19 severity. Targeting the renin-angiotensin-aldosterone system, particularly angiotensin-converting enzyme 2 (ACE2), may mitigate lung injury and excessive blood clotting in COVID-19 patients.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Pharmacology
Background:
- Comorbidities like hypertension significantly increase COVID-19 severity and mortality.
- Hypertension and the renin-angiotensin-aldosterone system (RAAS) contribute to vascular inflammation and endothelial dysfunction (ED), key factors in COVID-19 pathogenesis.
- Angiotensin-converting enzyme 2 (ACE2) is the cellular receptor for SARS-CoV-2 and a critical component of the RAAS.
Purpose of the Study:
- To investigate the role of RAAS, specifically ACE2, in COVID-19 severity.
- To explore the potential therapeutic benefits of targeting ACE2 and related pathways in managing COVID-19.
- To understand how targeting ED can alleviate COVID-19 symptoms and reduce fatalities.
Main Methods:
- Review of existing literature on hypertension, RAAS, ACE2, and COVID-19.
- Analysis of the mechanistic links between RAAS inhibition, ACE2 expression, and SARS-CoV-2 infection.
- Examination of the role of endothelial dysfunction and hypercoagulation in COVID-19 pathogenesis.
Main Results:
- RAAS inhibitors (ACE inhibitors, ARBs) may enhance ACE2 expression, potentially reducing lung injury.
- Increased ACE2 activity could decrease angiotensin II levels, mitigating inflammation and viral entry.
- COVID-19 is characterized by excessive blood clotting, highlighting the importance of coagulation pathways.
Conclusions:
- Targeting ACE2 presents a promising therapeutic strategy for SARS-CoV-2 infection and associated injuries.
- Modulating the RAAS pathway may help reverse COVID-19-induced hypercoagulation and reduce mortality.
- Further research into recombinant human ACE2 and anti-spike monoclonal antibodies is crucial for clinical application.
Abstract:
It is hypothesized that several comorbidities increase the severity of COVID-19 symptoms. Cardiovascular disease including hypertension was shown to play a critical role in the severity of COVID-19 infection by affecting the survival of patients with COVID-19. Hypertension and the renin-angiotensin-aldosterone system are involved in increasing vascular inflammation and endothelial dysfunction (ED), and both processes are instrumental in COVID-19. Angiotensin-converting enzyme 2 is an essential component of the renin-angiotensin-aldosterone system and the target receptor that mediates SARS-CoV-2 entry to the cell. This led to speculations that major renin-angiotensin-aldosterone system inhibitors, such as angiotensin receptor blockers and angiotensin-converting enzyme inhibitors might affect the course of the disease, since their administration enhances angiotensin-converting enzyme (ACE)2 expression. An increase in ACE2 activity could reduce angiotensin II concentration in the lungs and mitigate virus-driven lung injury. This could also be associated with a reduction in blood coagulation, which plays a critical role in the pathogenesis of SARS-CoV-2; of note, COVID-19 is now regarded as a disorder of blood clotting. Therefore, there is an urgent need to better understand the effect of targeting ACE2 as a potential treatment for SARS-CoV-2 driven injury, and in alleviating COVID-19 symptoms by reversing SARS-CoV-2-induced excessive coagulation and fatalities. Ongoing therapeutic strategies that include recombinant human ACE2 and anti-spike monoclonal antibodies are essential for future clinical practice in order to better understand the effect of targeting ED in COVID-19.
