tetano
Editor, Senior Moderator
Nat Commun
. 2024 May 20;15(1):3816.
doi: 10.1038/s41467-024-48055-0. Fatal COVID-19 pulmonary disease involves ferroptosis
Baiyu Qiu[SUP] #[/SUP][SUP] 1 [/SUP], Fereshteh Zandkarimi[SUP] #[/SUP][SUP] 1 2 [/SUP], Anjali Saqi[SUP] #[/SUP][SUP] 3 [/SUP], Candace Castagna[SUP] 4 [/SUP], Hui Tan[SUP] 1 [/SUP], Miroslav Sekulic[SUP] 3 [/SUP], Lisa Miorin[SUP] 5 6 [/SUP], Hanina Hibshoosh[SUP] 3 [/SUP], Shinya Toyokuni[SUP] 7 8 [/SUP], Koji Uchida[SUP] 9 [/SUP], Brent R Stockwell[SUP] 10 11 12 [/SUP]
Affiliations
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.
. 2024 May 20;15(1):3816.
doi: 10.1038/s41467-024-48055-0. Fatal COVID-19 pulmonary disease involves ferroptosis
Baiyu Qiu[SUP] #[/SUP][SUP] 1 [/SUP], Fereshteh Zandkarimi[SUP] #[/SUP][SUP] 1 2 [/SUP], Anjali Saqi[SUP] #[/SUP][SUP] 3 [/SUP], Candace Castagna[SUP] 4 [/SUP], Hui Tan[SUP] 1 [/SUP], Miroslav Sekulic[SUP] 3 [/SUP], Lisa Miorin[SUP] 5 6 [/SUP], Hanina Hibshoosh[SUP] 3 [/SUP], Shinya Toyokuni[SUP] 7 8 [/SUP], Koji Uchida[SUP] 9 [/SUP], Brent R Stockwell[SUP] 10 11 12 [/SUP]
Affiliations
- PMID: 38769293
- DOI: 10.1038/s41467-024-48055-0
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.