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Endothelial Dysfunction, Inflammation, and Oxidative Stress in COVID-19-Mechanisms and Therapeutic Targets

Adriana Fodor1, Brandusa Tiperciuc2, Cezar Login3

  • 1Clinical Center of Diabetes, Nutrition, and Metabolic Diseases, "Iuliu Haţieganu" University of Medicine and Pharmacy, 400012 Cluj-Napoca, CJ, Romania.

Oxidative Medicine and Cellular Longevity
|August 30, 2021
PubMed

Insights

COVID-19, caused by SARS-CoV-2, affects the cardiovascular system and lungs, leading to respiratory failure. This review highlights endothelial dysfunction as a key factor in COVID-19 pathogenesis.

Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Pathology

Background:

  • COVID-19 pandemic is a global health crisis with high mortality.
  • SARS-CoV-2 infection impacts both pulmonary and cardiovascular systems.
  • Severe COVID-19 involves respiratory failure due to alveolar damage and vascular complications.

Purpose of the Study:

  • To review the central role of endothelial dysfunction in COVID-19 pathogenesis.
  • To explore the mechanisms linking endotheliopathy to COVID-19 severity.
  • To identify therapeutic targets arising from COVID-19-associated endotheliopathy.

Main Methods:

  • Literature review of studies on COVID-19 pathophysiology.
  • Analysis of mechanisms of lung and cardiovascular damage in SARS-CoV-2 infection.
  • Synthesis of current understanding of endothelial involvement in COVID-19.

Main Results:

  • COVID-19 is increasingly recognized as an endothelial disease.
  • Endotheliopathy contributes to inflammation, cytokine storm, oxidative stress, and coagulopathy.
  • Vascular involvement, both macro- and microvascular, is crucial in severe COVID-19.

Conclusions:

  • Endothelial dysfunction is a critical factor in COVID-19 pathogenesis.
  • Targeting endotheliopathy offers potential therapeutic strategies for COVID-19.
  • Understanding the endothelial basis of COVID-19 is vital for clinical management.

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