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COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells
Stanislovas S Jankauskas1, Urna Kansakar1, Celestino Sardu2
1Department of Medicine, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA.
Insights
Serum from patients who did not survive COVID-19 significantly increased lipid peroxidation and ferroptosis markers in human endothelial cells, highlighting a link between disease severity and cellular damage.
Area of Science:
- Biomedical Science
- Cell Biology
- Pathophysiology
Background:
- COVID-19 (coronavirus disease 2019) pathophysiology involves oxidative stress and endothelial dysfunction.
- Lipid peroxidation and ferroptosis are critical cellular processes implicated in disease severity.
Purpose of the Study:
- To investigate the impact of COVID-19 on lipid peroxidation and ferroptosis in human endothelial cells.
- To determine if COVID-19-induced oxidative stress and lipid peroxidation correlate with patient outcomes.
Main Methods:
- Human endothelial cells were incubated with serum from COVID-19 patients (survivors vs. non-survivors).
- Assessed reactive oxygen species (ROS) generation and lipid peroxidation.
- Analyzed expression levels of ferroptosis markers (GPX4, SLC7A11, FTH1, SAT1).
- Investigated the role of TNFR1 by silencing it in endothelial cells.
Main Results:
- Serum from non-survivors significantly increased lipid peroxidation in endothelial cells.
- Non-survivor serum markedly altered expression of key ferroptosis markers.
- TNFR1 silencing rescued the ferroptosis-related gene expression changes.
Conclusions:
- Serum from non-surviving COVID-19 patients induces lipid peroxidation in human endothelial cells.
- These findings suggest a mechanism linking COVID-19 severity to endothelial cell damage via lipid peroxidation and ferroptosis.
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.
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