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Updated: Aug 30, 2025
Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
Vascular Aging and COVID-19
Ignas Badaras1, Agnė Laučytė-Cibulskienė2,3
1Faculty of Medicine, 54694Vilnius University, Vilnius, Lithuania.
Insights
Vascular aging, characterized by arterial wall changes, predicts mortality. Coronavirus disease 2019 (COVID-19) shares pathways with vascular aging, necessitating research into its long-term vascular health effects.
Area of Science:
- Cardiovascular Science
- Vascular Biology
- Infectious Disease
Background:
- Vascular age, assessed by pulse wave velocity, predicts mortality and reflects arterial wall health.
- Cellular senescence, oxidative stress, and endothelial dysfunction are key mechanisms in vascular aging.
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) impacts the vascular endothelium via direct and indirect mechanisms.
Purpose of the Study:
- To explore the shared pathways between vascular aging and coronavirus disease 2019 (COVID-19).
- To highlight the need for research on the long-term vascular health consequences of COVID-19.
Main Methods:
- Review of existing literature on vascular aging mechanisms.
- Analysis of SARS-CoV-2 interaction with endothelial cells, including ACE-2 receptor involvement.
- Comparison of cellular and molecular pathways implicated in both vascular aging and COVID-19.
Main Results:
- Vascular aging involves endothelial dysfunction, increased stiffness, and calcification.
- SARS-CoV-2 infection can lead to endothelial damage through hyperinflammation and ACE-2 receptor disruption.
- Shared pathways include oxidative stress and endothelial dysfunction.
Conclusions:
- COVID-19 and vascular aging share common pathophysiological mechanisms.
- Understanding these shared pathways is crucial for assessing long-term vascular health after COVID-19 infection.
- Further research is essential to elucidate the long-term vascular sequelae of SARS-CoV-2.
Abstract:
Vascular age is determined by functional and structural changes in the arterial wall. When measured by its proxy, pulse wave velocity, it has been shown to predict cardiovascular and total mortality. Disconcordance between chronological and vascular age might represent better or worse vascular health. Cell senescence is caused by oxidative stress and sustained cell replication. Senescent cells acquire senescence-associated secretory phenotype. Oxidative stress, endothelial dysfunction, dysregulation of coagulation and leucocyte infiltration are observed in the aging endothelium. All of these mechanisms lead to increased vascular calcification and stiffness. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can involve the vascular endothelium. It enters cells using angiotensin-converting enzyme 2 (ACE-2) receptors, which are abundant in endothelial cells. The damage this virus does to the endothelium can be direct or indirect. Indirect damage is caused by hyperinflammation. Direct damage results from effects on ACE-2 receptors. The reduction of ACE-2 levels seen during coronavirus disease 2019 (COVID-19) infection might cause vasoconstriction and oxidative stress. COVID-19 and vascular aging share some pathways. Due to the novelty of the virus, there is an urgent need for studies that investigate its long-term effects on vascular health.
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