Iron: Innocent bystander or vicious culprit in COVID-19 pathogenesis?

Marvin Edeas*, Jumana Saleh, Carole Peyssonnaux

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

10 Citations (Scopus)

Abstract

The coronavirus 2 (SARS-CoV-2) pandemic is viciously spreading through the continents with rapidly increasing mortality rates. Current management of COVID-19 is based on the premise that respiratory failure is the leading cause of mortality. However, mounting evidence links accelerated pathogenesis in gravely ill COVID-19 patients to a hyper-inflammatory state involving a cytokine storm. Several components of the heightened inflammatory state were addressed as therapeutic targets. Another key component of the heightened inflammatory state is hyper-ferritinemia which reportedly identifies patients with increased mortality risk. In spite of its strong association with mortality, it is not yet clear if hyper-ferritinemia in COVID-19 patients is merely a systemic marker of disease progression, or a key modulator in disease pathogenesis. Here we address implications of a possible role for hyper-ferritinemia, and altered iron homeostasis in COVID-19 pathogenesis, and potential therapeutic targets in this regard.

Original languageEnglish
Pages (from-to)303-305
Number of pages3
JournalInternational Journal of Infectious Diseases
Volume97
DOIs
Publication statusPublished - Aug 1 2020

Keywords

  • Ferroptosis
  • Hyper-ferritinemia
  • Hypercoagulability
  • Iron homeostasis
  • Mitochondria
  • Oxidative stress

ASJC Scopus subject areas

  • Microbiology (medical)
  • Infectious Diseases

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