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Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease
Microplastics may worsen cell damage by increasing harmful molecules and recycling processes in chronic lung disease
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Abstract
Concentrations of microplastics, particularly polystyrene microplastics, were significantly higher in the lung tissues of COPD patients compared to controls.
- Microplastics may induce mitochondrial dysfunction and iron accumulation, which are associated with autophagy-dependent .
- In vitro and in vivo experiments suggest that microplastics can enhance inflammation in COPD.
- Exposure to 2 μm polystyrene microplastics leads to their deposition in the lungs of COPD model mice.
- Mitochondrial impairments and overproduction of occur alongside increased lysosome biogenesis in response to microplastic exposure.
- Alleviating excessive inflammation and acute exacerbation of COPD may be possible through targeting autophagy-dependent ferroptosis.
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Key numbers
7 of 13 patients
Increased microplastics concentration
Patients with COPD had significantly higher microplastics in lung tissues compared to healthy controls.
200 μg/ml
Cell death threshold
Significant cell death in primary bronchial epithelial cells occurred at this concentration of PS-MPs.
50 μg/ml
Mito-ROS increase
Mito-ROS levels began to rise significantly at this concentration of PS-MPs stimulation.