COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells

Stanislovas S. Jankauskas, Urna Kansakar, Celestino Sardu, Fahimeh Varzideh, Roberta Avvisato, Xujun Wang, Alessandro Matarese, Raffaele Marfella, Marcello Ziosi, Jessica Gambardella, Gaetano Santulli

Research output: Contribution to journalArticlepeer-review

35 Scopus citations

Abstract

Oxidative stress and endothelial dysfunction have been shown to play crucial roles in the pathophysiology of COVID-19 (coronavirus disease 2019). On these grounds, we sought to investigate the impact of COVID-19 on lipid peroxidation and ferroptosis in human endothelial cells. We hypothesized that oxidative stress and lipid peroxidation induced by COVID-19 in endothelial cells could be linked to the disease outcome. Thus, we collected serum from COVID-19 patients on hospital admission, and we incubated these sera with human endothelial cells, comparing the effects on the generation of reactive oxygen species (ROS) and lipid peroxidation between patients who survived and patients who did not survive. We found that the serum from non-survivors significantly increased lipid peroxidation. Moreover, serum from non-survivors markedly regulated the expression levels of the main markers of ferroptosis, including GPX4, SLC7A11, FTH1, and SAT1, a response that was rescued by silencing TNFR1 on endothelial cells. Taken together, our data indicate that serum from patients who did not survive COVID-19 triggers lipid peroxidation in human endothelial cells.

Original languageEnglish (US)
Article number326
JournalAntioxidants
Volume12
Issue number2
DOIs
StatePublished - Feb 2023

Keywords

  • COVID-19
  • HUVEC
  • ROS
  • SARS-CoV-2
  • endothelial dysfunction
  • ferroptosis
  • inflammation
  • lipid peroxidation
  • long COVID
  • oxidative stress
  • oxytosis
  • peroxidation

ASJC Scopus subject areas

  • Food Science
  • Physiology
  • Biochemistry
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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