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Polystyrene microplastics-induced macrophage extracellular traps contributes to liver fibrotic injury by activating ROS/TGF-β/Smad2/3 signaling axis
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In a mouse study, polystyrene microplastics caused liver scarring (fibrosis) by triggering immune cells called macrophages to release web-like traps that promoted inflammation. Smaller microplastic particles caused more severe liver damage than larger ones, and the damage involved a specific signaling pathway (ROS/TGF-beta/Smad2/3) that drives tissue scarring. This research reveals a new mechanism by which microplastics may contribute to chronic liver disease.
Microplastics (MPs) are a type of emerging pollutant, posing a great threat to human and animal health. While recent studies have revealed the link between MPs exposure and liver injury of organisms, the effect of particle size on the level of MPs-induced hepatotoxicity and the intrinsic mechanism remain to be explored. Here, we established a mouse model exposed to two-diameter polystyrene MPs (PS-MPs, 1-10 μm or 50-100 μm) for 30 days. The in vivo results revealed that PS-MPs caused liver fibrotic injury in mice, accompanied with macrophages recruitment and macrophage extracellular traps (METs) formation, which were negatively correlated with particle size. The data in vitro showed that PS-MPs treatment could induce macrophages to release METs in a reactive oxygen species (ROS)-independent manner, and the METs formation level caused by large-size particles was higher than small-size particles. Further mechanistic analysis of a cell co-culture system revealed that PS-MPs-induced METs release led to a hepatocellular inflammatory response and epithelial-mesenchymal transition (EMT) via activating the ROS/TGF-β/Smad2/3 signaling axis, and this biological crosstalk could be relieved by DNase I. Overall, this findings demonstrates the key role of the action mechanism of METs in aggravating MPs-caused liver injury.
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Polystyrene microplastics promote liver inflammation by inducing the formation of macrophages extracellular traps
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Researchers discovered that polystyrene microplastics trigger liver inflammation by causing immune cells called macrophages to release web-like structures (extracellular traps) that damage surrounding liver cells. The mechanism involves microplastics generating harmful reactive oxygen species inside macrophages, disrupting their internal recycling systems and ultimately causing them to burst, which highlights how microplastics may drive organ inflammation in the body.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
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In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
Accumulation of polystyrene microplastics induces liver fibrosis by activating cGAS/STING pathway
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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.
Polystyrene microplastics and hepatic fibrosis-related indices in type 2 diabetes: a cross-sectional analysis with experimental validation
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Researchers found that polystyrene microplastics detected in blood were the polymer most consistently linked to elevated liver fibrosis markers in type 2 diabetic patients, and confirmed in diabetic mice that PS-MPs worsen hepatic steatosis and fibrosis by activating the NLRP3 inflammasome and TGF-β1/Smad signaling pathways.
PS-MPs Induced Inflammation and Phosphorylation of Inflammatory Signalling Pathways in Liver
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Polystyrene microplastics (0.1 µm) induced inflammatory responses and activated multiple inflammatory signalling pathways in mouse and human liver cell lines after 28 days of exposure. The study identified specific phosphorylation cascades through which PS MPs trigger hepatic inflammation, linking microplastic exposure to liver damage mechanisms.
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