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Updated: Aug 1, 2025

Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
Damage to endothelial barriers and its contribution to long COVID
Xiaoming Wu1, Mengqi Xiang1, Haijiao Jing1
1Department of Hematology, The First Hospital, Harbin Medical University, 150001, Harbin, China.
Insights
Endothelial injury and dysfunction are key drivers of severe COVID-19 and long COVID. This review explores how damage to endothelial barriers in various organs contributes to persistent symptoms after SARS-CoV-2 infection.
Area of Science:
- Cardiovascular Biology
- Infectious Diseases
- Pathology
Background:
- COVID-19, caused by SARS-CoV-2, presents ongoing global health challenges, exacerbated by emerging viral variants.
- A significant portion of individuals recovering from acute infection develop persistent symptoms, termed long COVID.
- Endothelial injury and dysfunction are consistently observed in both acute COVID-19 and convalescent patients across multiple study types.
Purpose of the Study:
- To elucidate the role of endothelial barriers in the pathogenesis of long COVID.
- To highlight the knowledge gap concerning organ-specific endothelial barrier damage and its sequelae.
- To review the mechanisms of endothelial injury and dysfunction in the context of SARS-CoV-2 infection.
Main Methods:
- Review of clinical, autopsy, animal, and in vitro studies.
- Analysis of the structural and functional changes in endothelial cells and barriers.
- Focus on the impact of endothelial barrier damage on different organ systems.
Main Results:
- Endothelial injury manifests as increased permeability, glycocalyx shedding, and barrier disruption.
- During acute SARS-CoV-2 infection, endothelial damage leads to microthrombi and multiple organ dysfunction.
- Persistent endothelial dysfunction in convalescence is a significant contributor to long COVID development.
Conclusions:
- Endothelial barriers play a critical role in the diverse manifestations of long COVID.
- Understanding organ-specific endothelial dysfunction is crucial for addressing long COVID.
- Targeting endothelial injury pathways may offer therapeutic strategies for long COVID recovery.
Abstract:
The world continues to contend with COVID-19, fueled by the emergence of viral variants. At the same time, a subset of convalescent individuals continues to experience persistent and prolonged sequelae, known as long COVID. Clinical, autopsy, animal and in vitro studies all reveal endothelial injury in acute COVID-19 and convalescent patients. Endothelial dysfunction is now recognized as a central factor in COVID-19 progression and long COVID development. Different organs contain different types of endothelia, each with specific features, forming different endothelial barriers and executing different physiological functions. Endothelial injury results in contraction of cell margins (increased permeability), shedding of glycocalyx, extension of phosphatidylserine-rich filopods, and barrier damage. During acute SARS-CoV-2 infection, damaged endothelial cells promote diffuse microthrombi and destroy the endothelial (including blood-air, blood-brain, glomerular filtration and intestinal-blood) barriers, leading to multiple organ dysfunction. During the convalescence period, a subset of patients is unable to fully recover due to persistent endothelial dysfunction, contributing to long COVID. There is still an important knowledge gap between endothelial barrier damage in different organs and COVID-19 sequelae. In this article, we mainly focus on these endothelial barriers and their contribution to long COVID.
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