ArticleLiver international : official journal of the International Association for the Study of the Liver2025
Chronic Nanoplastic Exposure Promotes the Development and Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Transcriptomic responses to repeated exposure of human C3A liver spheroids to polystyrene nanoplastics.Archives of toxicology · 2026Article
- Microplastics, nanoplastics and liver disease: an emerging health concern?Nature reviews. Gastroenterology & hepatology · 2026Review
- Micro- and Nanoplastics as Emerging Drivers of Liver Injury: Exposure, Evidence, and Mechanisms.International journal of molecular sciences · 2026Review
- Review
- Chronic Nanoplastic Exposure Promotes the Development and Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
BACKGROUND AND
aimsPlastic particles are a global pollution problem, and humans are potentially exposed to them. Ingested plastic particles, microparticles (MPs) and nanoparticles (NPs), predominantly accumulate in the liver and cause hepatotoxicity through oxidative stress and metabolic dysfunction. NPs promote more toxic actions than MPs; however, the mechanisms involved in developing and progressing metabolic dysfunction-associated steatotic liver disease (MASLD) from chronic exposure to NPs remain poorly understood. Hedgehog (Hh) signalling regulates MASLD pathogenesis. Herein, we investigated the pathophysiological effects of NPs in MASLD.
methodsMice were orally administered NPs via drinking water while fed a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) for 12 weeks.
resultsNPs increased lipid accumulation in hepatocytes and apoptosis. Moreover, these actions were enhanced in lipotoxicity-exposed hepatocytes. Chronically exposed NPs accumulated in mice livers and aggravated CDAHFD-induced hepatic damage, especially fibrosis. Activated Hh signalling in the CDAHFD group was elevated by NP treatment. Increased Sonic Hh expression in the hepatocytes of NP-treated mice in the CDAHFD group triggered Hh signalling in hepatic stellate cells (HSCs), which promoted liver fibrosis.
conclusionsThese results demonstrate that chronic exposure to NPs increases vulnerability to MASLD progression, suggesting that NPs are a potentially harmful factor in the development and progression of liver disease.
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