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Updated: Oct 13, 2025
Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
The Role of Endothelium in COVID-19
Mihaela Ionescu1, Anca Pantea Stoian2, Manfredi Rizzo2,3
1Cardiology Department, Faculty of Medicine, Ovidius University of Constanţa, 900527 Constanţa, Romania.
Insights
Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) causes cardiovascular issues by damaging endothelial cells. This review explores endothelial dysfunction in COVID-19 patients with cardiometabolic diseases and potential treatments.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Pathophysiology
Background:
- The COVID-19 pandemic, caused by SARS-CoV-2, presents significant cardiovascular risks.
- Pre-existing cardiovascular comorbidities are prevalent in severe COVID-19 cases.
- SARS-CoV-2 infection triggers hyperinflammation, hypoxia, and endothelial cell dysfunction.
Purpose of the Study:
- To review the role of endothelial dysfunction in COVID-19 pathogenesis.
- To examine the impact of COVID-19 on patients with cardiometabolic diseases.
- To discuss potential therapeutic strategies for severe COVID-19.
Main Methods:
- Literature review of recent findings on COVID-19 and cardiovascular complications.
- Analysis of SARS-CoV-2 mechanisms affecting endothelial cells.
- Focus on cardiometabolic disease interactions.
Main Results:
- Endothelial dysfunction is a key mechanism in COVID-19, leading to impaired organ perfusion.
- COVID-19 can cause acute myocardial injury, renal failure, and thromboembolic events.
- Cardiometabolic diseases exacerbate SARS-CoV-2-induced endothelial dysfunction.
Conclusions:
- Endothelial dysfunction is central to the severe manifestations of COVID-19, particularly in patients with cardiometabolic conditions.
- Understanding these mechanisms is crucial for developing effective treatments.
- Targeting endothelial dysfunction may mitigate COVID-19 severity.
Abstract:
The 2019 novel coronavirus, known as severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) or coronavirus disease 2019 (COVID-19), is causing a global pandemic. The virus primarily affects the upper and lower respiratory tracts and raises the risk of a variety of non-pulmonary consequences, the most severe and possibly fatal of which are cardiovascular problems. Data show that almost one-third of the patients with a moderate or severe form of COVID-19 had preexisting cardiovascular comorbidities such as diabetes mellitus, obesity, hypertension, heart failure, or coronary artery disease. SARS-CoV2 causes hyper inflammation, hypoxia, apoptosis, and a renin-angiotensin system imbalance in a variety of cell types, primarily endothelial cells. Profound endothelial dysfunction associated with COVID-19 can be the cause of impaired organ perfusion that may generate acute myocardial injury, renal failure, and a procoagulant state resulting in thromboembolic events. We discuss the most recent results on the involvement of endothelial dysfunction in the pathogenesis of COVID-19 in patients with cardiometabolic diseases in this review. We also provide insights on treatments that may reduce the severity of this viral infection.
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