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COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells
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 o...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9952002/ https://www.ncbi.nlm.nih.gov/pubmed/36829885 http://dx.doi.org/10.3390/antiox12020326 |
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author | Jankauskas, Stanislovas S. Kansakar, Urna Sardu, Celestino Varzideh, Fahimeh Avvisato, Roberta Wang, Xujun Matarese, Alessandro Marfella, Raffaele Ziosi, Marcello Gambardella, Jessica Santulli, Gaetano |
author_facet | Jankauskas, Stanislovas S. Kansakar, Urna Sardu, Celestino Varzideh, Fahimeh Avvisato, Roberta Wang, Xujun Matarese, Alessandro Marfella, Raffaele Ziosi, Marcello Gambardella, Jessica Santulli, Gaetano |
author_sort | Jankauskas, Stanislovas S. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9952002 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99520022023-02-25 COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells Jankauskas, Stanislovas S. Kansakar, Urna Sardu, Celestino Varzideh, Fahimeh Avvisato, Roberta Wang, Xujun Matarese, Alessandro Marfella, Raffaele Ziosi, Marcello Gambardella, Jessica Santulli, Gaetano Antioxidants (Basel) Article 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. MDPI 2023-01-31 /pmc/articles/PMC9952002/ /pubmed/36829885 http://dx.doi.org/10.3390/antiox12020326 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Jankauskas, Stanislovas S. Kansakar, Urna Sardu, Celestino Varzideh, Fahimeh Avvisato, Roberta Wang, Xujun Matarese, Alessandro Marfella, Raffaele Ziosi, Marcello Gambardella, Jessica Santulli, Gaetano COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells |
title | COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells |
title_full | COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells |
title_fullStr | COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells |
title_full_unstemmed | COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells |
title_short | COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells |
title_sort | covid-19 causes ferroptosis and oxidative stress in human endothelial cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9952002/ https://www.ncbi.nlm.nih.gov/pubmed/36829885 http://dx.doi.org/10.3390/antiox12020326 |
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