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Accumulation of polystyrene microplastics induces liver fibrosis by activating cGAS/STING pathway
Summary
Researchers found that tiny polystyrene microplastics (0.1 micrometers) can enter liver cells and cause DNA damage that triggers a chain reaction leading to liver scarring, known as fibrosis. The microplastics activated a specific immune signaling pathway called cGAS/STING, which caused inflammation that progressively damaged liver tissue even at low concentrations. This study reveals a specific mechanism by which long-term microplastic exposure could lead to serious liver disease in humans.
The environmental pollution from microplastics has caused concern from the whole society due to its harm to organisms. However, the effect of microplastics on liver damage and fibrosis remains unclear in the case of long-term accumulation. The present study demonstrated that the 0.1 μm microplastic could enter hepatocytes from circulation and result liver damage even at a low concentration. Microplastic exposure could induce DNA damage in both nucleus and mitochondria, by which the dsDNA fragment was translocated into cytoplasm and triggered the DNA sensing adaptor STING. The activation of cGAS/STING pathway initiated the downstream cascade reaction, the NFκB translocated into nucleus and upregulated pro-inflammatory cytokines expression, and thus facilitating liver fibrosis eventually. Furthermore, inhibition of STING could alleviate the liver fibrosis via blocking the NFκB translocation and fibronectin expression. This study provided a valuable insight to elucidate the potential risk and mechanism of hepatic toxicity and fibrosis induced by microplastics.
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