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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
07:56

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

Published on: May 5, 2023

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Complement-mediated microvascular injury and thrombosis in the pathogenesis of severe COVID-19: A review

Panagiota Gianni1, Mark Goldin2,3, Sam Ngu2

  • 1Department of Internal Medicine III, Hematology, Oncology, Palliative Medicine, Rheumatology and Infectious Diseases, University Hospital Ulm, Ulm 89070, Germany.

World Journal of Experimental Medicine
|September 26, 2022
PubMed

Insights

Excessive complement activation in COVID-19 drives thromboinflammation and microvascular thrombosis, increasing mortality. Complement inhibitors are explored as potential therapeutics to mitigate these severe complications.

Area of Science:

  • Immunology
  • Pathophysiology
  • Vascular Biology

Background:

  • Coronavirus disease 2019 (COVID-19) is associated with severe microvascular thrombosis, contributing to high mortality.
  • The underlying mechanisms involve excessive complement activation, leading to a cytokine storm and prothrombotic complications.
  • Thromboinflammation, characterized by inflammation and coagulation cascade activation, is a key aspect of COVID-19 pathogenesis.

Purpose of the Study:

  • To review the role of the complement system in COVID-19-associated thrombotic microangiopathy.
  • To summarize current data on complement inhibitors as potential therapeutics for COVID-19.

Main Methods:

  • Literature review of studies on COVID-19, complement activation, thrombosis, and thromboinflammation.
  • Analysis of evidence linking complement pathways to COVID-19 pathogenesis and thrombotic events.
  • Summary of clinical trial data and preclinical research on complement inhibitors in COVID-19.

Main Results:

  • The complement system significantly contributes to COVID-19-induced thromboinflammation and microvascular damage.
  • Excessive complement activation exacerbates inflammatory responses and tissue damage, promoting thrombosis.
  • Several complement inhibitors show promise in preclinical and early clinical studies for managing COVID-19 complications.

Conclusions:

  • The complement system is a critical mediator in the development of thrombotic microangiopathy in COVID-19.
  • Targeting the complement system with inhibitors represents a promising therapeutic strategy for COVID-19.
  • Further research is warranted to establish the efficacy and safety of complement inhibitors in clinical practice for COVID-19 treatment.

Keywords:
COVID-19ComplementCytokine stormMicrovascular injuryThromboembolismThrombotic microangiopathy

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