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Spatial Ppara-Anxa2 Axis in Polyethyelen-Driven Liver Damage
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Researchers used spatial transcriptomics to map how polyethylene microplastics disrupt liver cell populations in mice, revealing inflammatory hotspots with reduced cellular diversity and identifying the Ppara-Anxa2 signaling axis as a key molecular driver of PE-associated liver damage.
Microplastics (MP) are increasingly recognized as an urgent global health concern, with mounting evidence linking their bioaccumulation to chronic disease risks. The liver, as a central organ for metabolic homeostasis and detoxification, is particularly sensitive to sustained MP exposure. However, the mechanisms underlying hepatic responses to polyethylene (PE), the most prevalent yet relatively understudied plastic type, remain poorly defined. Spatial transcriptomics uncovered the cell-type heterogeneity and gene expression patterns masked in bulk analyses. Spatial clustering uncovered inflammatory hotspots characterized by reduced cellular diversity and distinct PE-responsive gene signatures. This study provides a molecular framework for understanding MP-associated disruption of liver pathophysiology and highlights potential targets for therapeutic intervention. Here we share the shinyapp versions. 1) Mouse_MP_Polyethylene_Hepatocytes_Cholangiocytes https://ohbiolab.shinyapps.io/shinyApp_MP_Polyethylene_Hepatocytes/ 2) Mouse_MP_Polyethylene_NonParenchymal https://ohbiolab.shinyapps.io/shinyApp_MP_Polyethylene_NonParenchymal/ 3) Mouse_MP_Polyethyelen_downsize_20pct (for better loading speed) https://ohbiolab.shinyapps.io/shinyApp_MP_Polyethylene_downsize_20pct/
More Papers Like This
Spatial Ppara-Anxa2 Axis in Polyethyelen-Driven Liver Damage
AI summary Read the abstract
Researchers used spatial transcriptomics to map how polyethylene microplastics disrupt liver cell populations in mice, revealing inflammatory hotspots with reduced cellular diversity and identifying the Ppara-Anxa2 signaling axis as a key molecular driver of PE-associated liver damage.
Spatial transcriptome mapping identifies Ppara-Anxa2 cross-talk in microplastic-induced hepatotoxicity
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Scientists studying mice found that exposure to polyethylene (a common plastic) microplastics disrupts liver function by throwing off a gene called Ppara, which normally helps control fat metabolism, and a related gene, Anxa2, that helps damaged tissue repair itself. Using detailed mapping technology that shows exactly where in the liver these changes happen, researchers spotted "hotspots" of inflammation and stress—offering a possible explanation for how microplastics might contribute to liver disease and pointing to genes that could one day be targeted by treatments. While this research was done in mice, it adds to growing evidence that
Single-cell transcriptome analysis of liver immune microenvironment changes induced by microplastics in mice with non-alcoholic fatty liver
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Using advanced single-cell analysis, researchers showed that microplastics worsened non-alcoholic fatty liver disease in mice fed a high-fat diet by changing how immune cells behaved in the liver. Microplastic exposure amplified inflammatory responses and altered the communication between different liver cell types. This study is important because it reveals specific immune mechanisms by which microplastics could worsen liver disease, a condition already affecting roughly one in four adults worldwide.
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This study examined how polypropylene microplastics accumulate in and damage the mouse liver, using integrated lipidomics and transcriptomics to map the molecular landscape of microplastic-induced lipid disruption and metabolic dysfunction.
Single-cell transcriptomic analysis reveals heterogeneity of the patterns of responsive genes and cell communications in liver cell populations of zebrafish exposed to polystyrene nanoplastics
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Researchers used single-cell gene analysis to examine how polystyrene nanoplastics affect different cell types in zebrafish livers. They discovered that various liver cell populations responded to nanoplastic exposure in distinctly different ways, with some cell types showing more disruption to fat metabolism and stress response genes than others. The study reveals that nanoplastic toxicity in the liver is not uniform and that certain cell populations may be more vulnerable than previously understood.
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