ArticlePloS one2024
Long-term exposure to polychlorinated biphenyl 126 induces liver fibrosis and upregulates miR-155 and miR-34a in C57BL/6 mice.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Changes and Relationships Between PCB 126, PCB 169 and Macroelement Concentrations During the Technological Process of Selected High-Fat Dairy Products.Molecules (Basel, Switzerland) · 2026Article
- Towards Bayesian-based quantitative adverse outcome pathways using in vitro data from open literature and continuous variables: a case example for liver fibrosis.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- PCB118 Is Associated with Impaired Decidualization and Angiogenesis Through miR-542-3p-Mediated Regulation of ILK Signaling.International journal of molecular sciences · 2026Article
- Review
- PCB-126 exposure promotes brown adipose tissue dysfunction and metabolic inflexibility in mice.Scientific reports · 2026Article
- Tributyl phosphate as a type of environmental endocrine disruptor associated with liver fibrosis: insights from NHANES andFrontiers in toxicology · 2025Article
- The Role of miRNAs and Epigenetic Factors in Non-Alcoholic Fatty Liver Disease - a Systematic Review.Current health sciences journalReview
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Authors and funding
9 authors.
Funding
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Abstract
Environmental pollutants, including polychlorinated biphenyls (PCBs), act as endocrine disruptors and impair various physiological processes. PCB 126 is associated with steatohepatitis, fibrosis, cirrhosis, and other hepatic injuries. These disorders can be regulated by microRNAs (miRNAs). Therefore, this study aimed to investigate the role of miRNAs in non-alcoholic fatty liver disease associated with exposure to PCB 126. Adult male C57BL/6 mice were exposed to PCB 126 (5 μmol/kg of body weight) for 10 weeks. The PCB group showed lipid accumulation in the liver in the presence of macro- and microvesicular steatosis and fibrosis with increased inflammatory and profibrotic gene expression, consistent with non-alcoholic steatohepatitis (NASH). PCB exposure also upregulated miR-155 and miR-34a, which induce the expression of proinflammatory cytokines and inflammation in the liver and reduce the expression of peroxisome proliferator-activated receptor α, which, in turn, impairs lipid oxidation and hepatic steatosis. Therefore, the present study showed that PCB 126 induced NASH via potential mechanisms involving miR-155 and miR-34a, which may contribute to the development of new diagnostic markers and therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.