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Ferritinophagy is involved in the zinc oxide nanoparticles-induced ferroptosis of vascular endothelial cells
Cell recycling of iron helps cause zinc oxide nanoparticle-triggered iron-dependent cell death in blood vessel lining cells
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Abstract
Zinc oxide nanoparticles (ZnONPs) induce in endothelial cells, leading to cell death.
- ZnONPs exposure increases intracellular iron levels and lipid peroxidation in a dose- and time-dependent manner.
- Cell death caused by ZnONPs can be attenuated by both a lipid reactive oxygen species scavenger and an iron chelator.
- Ferroptosis induced by ZnONPs depends on macroautophagy, as inhibiting autophagy reduces cell death.
- NCOA4-mediated is necessary for ZnONPs-induced ferroptosis, as its knockdown decreases iron levels and lipid peroxidation.
- Mitochondrial reactive oxygen species may activate the AMPK-ULK1 pathway to promote ferritinophagy.
- Pulmonary exposure to ZnONPs results in vascular inflammation and ferritinophagy in mice, with ferrostatin-1 mitigating vascular injury.
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Key numbers
MDA content
Increase in lipid peroxidation
Measured in HUVECs and EA.hy926 cells after ZnONPs treatment.
12 μg/mice
12 μg
Administered to mice during pulmonary exposure experiments.