tetano
Editor, Senior Moderator
Int J Infect Dis
. 2020 Jun 1;S1201-9712(20)30417-3.
doi: 10.1016/j.ijid.2020.05.110. Online ahead of print.
Iron: Innocent Bystander or Vicious Culprit in COVID-19 Pathogenesis?
Marvin Edeas[SUP] 1 [/SUP], Jumana Saleh[SUP] 2 [/SUP], Carole Peyssonnaux[SUP] 3 [/SUP]
Affiliations
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 that respiratory failure is the leading cause of mortality. However, mounting evidence link 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.
Keywords: Ferroptosis; Hyper-Ferritinemia; Hypercoagulability; Iron Homeostasis; Mitochondria; Oxidative Stress.
. 2020 Jun 1;S1201-9712(20)30417-3.
doi: 10.1016/j.ijid.2020.05.110. Online ahead of print.
Iron: Innocent Bystander or Vicious Culprit in COVID-19 Pathogenesis?
Marvin Edeas[SUP] 1 [/SUP], Jumana Saleh[SUP] 2 [/SUP], Carole Peyssonnaux[SUP] 3 [/SUP]
Affiliations
- PMID: 32497811
- DOI: 10.1016/j.ijid.2020.05.110
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 that respiratory failure is the leading cause of mortality. However, mounting evidence link 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.
Keywords: Ferroptosis; Hyper-Ferritinemia; Hypercoagulability; Iron Homeostasis; Mitochondria; Oxidative Stress.