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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis

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Potential role of endothelial cell surface ectopic redox complexes in COVID-19 disease pathogenesis

Isabella Panfoli1

  • 1University of Genoa, Genoa, Italy panfoli@difar.unige.it.

Clinical Medicine (London, England)
|July 1, 2020
PubMed

Insights

COVID-19 may be an endothelial disease where the virus damages cells, increasing oxidative stress and leading to blood clots and inflammation. Oxygen availability might influence disease severity.

Area of Science:

  • Cardiovascular Science
  • Infectious Diseases
  • Pathology

Background:

  • COVID-19 presents significant challenges in understanding its pathogenesis and treatment.
  • Emerging evidence suggests COVID-19 may primarily affect the endothelium (the inner lining of blood vessels).
  • The virus binds to angiotensin-converting enzyme type 2 (ACE2), prevalent on endothelial cells.

Purpose of the Study:

  • To explore the role of endothelial dysfunction and oxidative stress in COVID-19 pathogenesis.
  • To investigate the link between viral damage, ACE2, and the development of thrombotic and inflammatory complications.

Main Methods:

  • This study is a conceptual review based on existing literature.
  • Analysis of the interaction between SARS-CoV-2, ACE2, and endothelial cell function.
  • Examination of the role of reactive oxygen species (ROS) and oxidative stress.

Main Results:

  • Viral binding to ACE2 can lead to endothelial dysfunction and increased ROS production.
  • Oxidative stress may promote a pro-thrombotic and pro-inflammatory state in endothelial cells.
  • This cellular state can predispose patients to thromboembolic events, vasculitis, and disseminated intravascular coagulopathy (DIC).

Conclusions:

  • COVID-19 exhibits characteristics of an endothelial disease.
  • Oxidative stress, driven by viral damage to ACE2-expressing endothelial cells, is a key pathogenetic factor.
  • Oxygen availability may modulate the severity of COVID-19 by influencing the oxidant state and cellular damage.

Keywords:
COVID-19ectopic electron transfer chainendotheliumoxidative stressoxygen

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