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Polystyrene microplastics induce liver fibrosis and lipid deposition in mice through three hub genes revealed by the RNA-seq
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A mouse study revealed that long-term exposure to polystyrene microplastics of different sizes caused liver scarring (fibrosis) and abnormal fat buildup in the liver. Genetic analysis identified three key genes driving this damage, with smaller microplastics causing more severe effects, providing new insight into how microplastic exposure may contribute to chronic liver disease.
Nano- and microplastics (NMPs) have become a serious global environmental threat that causes damage to mammalian organs. In this work, we investigated the potential molecular mechanism underlying the development of liver fibrosis induced by long-term exposure to three different sized polystyrene (PS)-NMPs (80 nm, 0.5 µm and 5 µm) in mice. Liver fibrosis levels were evaluated in mice after chronic exposure to PS-NMPs. Liver inflammation was mainly increased in chronic exposure to 80 nm and 0.5 µm PS-NMPs. Liver lipid deposition was significantly enhanced after PS-NMPs exposure. However, oxidative stress was not changed under PS-NMPs exposure. GO enrichment and KEGG pathway analyses revealed that the DEGs and shared DEGs were mainly enriched in the metabolism of lipids. The mRNA expression levels of genes related to fatty acid oxidation, synthesis and transport were dramatically induced by PS-NMPs exposure. Four hub genes, Acot3, Abcc3, Nr1i3 and Fmo2, were identified by CytoHubba analysis of shared DEGs. The mRNA expression levels of three hub genes, Acot3, Abcc3 and Nr1i3, were significantly augmented under chronic PS-NMPs exposure. Our results suggest that Acot3, Abcc3 and Nr1i3 are potential molecules involved in the development of liver fibrosis under chronic exposure to PS-NMPs.
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A mouse study found that long-term exposure to polystyrene microplastics increased the risk of developing non-alcoholic fatty liver disease. The microplastics accumulated in the liver and disrupted fat metabolism, causing inflammation and liver damage, which is concerning because most previous studies only looked at short-term exposure effects.
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