COVID-19-driven endothelial damage: complement, HIF-1, and ABL2 are potential pathways of damage and targets for cure

Monia Marchetti1

  • 1Hematology Department, Az Osp SS Antonio e Biagio e Cesare Arrigo, Alessandria, Italy. moniamarchettitamellini@gmail.com.

Annals of Hematology
|June 26, 2020
PubMed

Insights

This review examines how COVID-19 causes organ damage through inflammation and endothelial dysfunction. It explores therapeutic targets and existing drugs like eculizumab for potential clinical trials.

Area of Science:

  • Cardiovascular Medicine
  • Virology
  • Immunology

Background:

  • COVID-19 pandemic presents a global health crisis with significant mortality.
  • High morbidity is linked to hypoxia and inflammation, causing endothelial dysfunction and coagulation issues.
  • Endothelial derangement affects both small and large blood vessels.

Purpose of the Study:

  • To review key pathways contributing to COVID-19-induced endothelial dysfunction.
  • To identify potential therapeutic targets for mitigating COVID-19-related organ damage.
  • To evaluate existing drugs for their suitability in clinical trials.

Main Methods:

  • Literature review focusing on molecular pathways.
  • Analysis of complement system, HIF-1α, and ABL tyrosine kinases in COVID-19.
  • Assessment of marketed drugs for therapeutic potential.

Main Results:

  • Identified complement, HIF-1α, and ABL tyrosine kinases as critical pathways in endothelial injury.
  • Highlighted potential molecular targets for intervention.
  • Eculizumab and imatinib identified as promising candidates for clinical trials.

Conclusions:

  • Understanding these pathways is crucial for managing COVID-19 complications.
  • Targeting endothelial dysfunction offers a promising therapeutic strategy.
  • Repurposing existing drugs may accelerate treatment development for COVID-19 organ damage.

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