ArticleJournal of advanced research2026
Hepatotoxicity induced by polylactic acid microplastics: The mediating role of gut microbiota and uric acid metabolism.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Gut-Mediated Systemic Toxicity of Micro- and Nanoplastics: Nanoscale Biointerface Properties, Microbiota-Metabolite Crosstalk, and Evidence Across Gut-Organ Axes.Nanomaterials (Basel, Switzerland) · 2026Review
- Degradation reshapes the toxic identity of polylactic acid microplastics through MSR1-dependent immune decoding in mouse kidney.Particle and fibre toxicology · 2026Article
- Bioplastics Toxicity upon Ingestion: A Critical Review of Biotransformation and Gastrointestinal Effects.Polymers · 2026Review
- Tumour-infiltrating microplastics disrupt the JAK-STAT-microbiota axis to promote immunotherapy resistance in colorectal cancer.Molecular cancer · 2026Article
- Pathogenesis of Micro/Nanoplastics in Mammalian Systems: Gut to Systemic Multi-Organ Dysfunction.Research (Washington, D.C.) · 2026Review
- Curcumin attenuates liver injury by modulating the AGE-RAGE axis and metabolic homeostasis in high-fat diet/streptozotocin-induced type 2 diabetic mice.Frontiers in nutrition · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe increasing use of biodegradable plastics has led to the inevitable human consumption of biodegradable microplastics (MPs). These MPs can be degraded and absorbed into various organs and tissues via the gastrointestinal tract, with the liver being the primary target for digestion and absorption.
objectivesThis study aimed to investigate the toxic effects and mechanisms of biodegradable MPs on the liver following gastrointestinal degradation.
methodsPolylactic acid (PLA) was used as a representative bioplastic. We simulated pristine and partially degraded states using polymeric and oligomeric PLA MPs. Mice were exposed to these MPs via 28-day repeated gavage administration at environmentally realistic concentrations. In vivo multi-omics analyses, combined with in vitro studies, were employed to explore underlying mechanisms.
resultsExposure to PLA oligomers and polymers disrupted gut microbiota, triggering an increase in plasma and hepatic uric acid levels in the mice. Elevated uric acid levels, in turn, upregulated the Hsd17b13 mRNA expression in the liver. This cascade was linked to an accumulation of hepatic triglycerides, triggering liver inflammation and promoting the progression of fibrosis. The clearance of the intestinal microbiota mitigated PLA MP-induced liver injury in mice. In HepG2 cells, PLA oligomers and polymers did not enhance the HSD17B13 mRNA expression or increase cellular lipid droplet formation. Conversely, the presence of uric acid upregulated the HSD17B13 and augmented lipid droplet production. Furthermore, simultaneous exposure to PLA particles and uric acid did not intensify lipid accumulation or lipid droplet formation within these cells.
conclusionOur findings demonstrate that PLA MP-induced liver damage is mediated by gut microbiota-driven elevation of uric acid. This highlights the critical role of systemic factors, particularly gut microbiota, in assessing the hepatotoxicity of PLA MPs.
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