Fatal COVID-19 pulmonary disease involves ferroptosis

Baiyu Qiu, Fereshteh Zandkarimi, Anjali Saqi, Candace Castagna, Hui Tan, Miroslav Sekulic, Lisa Miorin, Hanina Hibshoosh, Shinya Toyokuni, Koji Uchida and Brent R. Stockwell ()
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Baiyu Qiu: Columbia University
Fereshteh Zandkarimi: Columbia University
Anjali Saqi: Columbia University Irving Medical Center
Candace Castagna: Columbia University Irving Medical Center
Hui Tan: Columbia University
Miroslav Sekulic: Columbia University Irving Medical Center
Lisa Miorin: Icahn School of Medicine at Mount Sinai
Hanina Hibshoosh: Columbia University Irving Medical Center
Shinya Toyokuni: Nagoya University Graduate School of Medicine
Koji Uchida: The University of Tokyo
Brent R. Stockwell: Columbia University

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract SARS-CoV-2 infection causes severe pulmonary manifestations, with poorly understood mechanisms and limited treatment options. Hyperferritinemia and disrupted lung iron homeostasis in COVID-19 patients imply that ferroptosis, an iron-dependent cell death, may occur. Immunostaining and lipidomic analysis in COVID-19 lung autopsies reveal increases in ferroptosis markers, including transferrin receptor 1 and malondialdehyde accumulation in fatal cases. COVID-19 lungs display dysregulation of lipids involved in metabolism and ferroptosis. We find increased ferritin light chain associated with severe COVID-19 lung pathology. Iron overload promotes ferroptosis in both primary cells and cancerous lung epithelial cells. In addition, ferroptosis markers strongly correlate with lung injury severity in a COVID-19 lung disease model using male Syrian hamsters. These results reveal a role for ferroptosis in COVID-19 pulmonary disease; pharmacological ferroptosis inhibition may serve as an adjuvant therapy to prevent lung damage during SARS-CoV-2 infection.

Date: 2024
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DOI: 10.1038/s41467-024-48055-0

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