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Micro- and Nanoplastics as Disruptors of Digestive and Hepatopancreatic Homeostasis: Insights into the Plastic-Gut-Liver Axis
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Researchers reviewed how micro- and nanoplastics disrupt the gut-liver axis by compromising intestinal barrier integrity, promoting microbiota dysbiosis, and enabling microbial translocation via portal circulation that triggers hepatic inflammation, metabolic reprogramming, and potential carcinogenic processes, while also noting emerging evidence of pancreatic and multi-organ involvement.
Micro- and nanoplastics (MPs/NPs) have emerged as pervasive environmental contaminants with increasing implications for human health, particularly within the digestive system. This review critically examines the role of MPs/NPs as disruptors of gastrointestinal and liver homeostasis through the lens of the plastic-gut-liver axis. We synthesize current evidence on primary exposure routes-including ingestion, inhalation, dermal contact, and transplacental transfer-and highlight their intestinal uptake, systemic dissemination, and tissue accumulation. Mechanistically, MPs/NPs compromise intestinal barrier integrity, promote oxidative stress, and induce microbiota dysbiosis, facilitating the translocation of microbial-derived signals to the liver via the portal circulation. This process triggers inflammatory signaling cascades, metabolic reprogramming, and immune dysregulation, contributing to hepatic steatosis, insulin resistance, and potential carcinogenic processes. Emerging evidence also implicates pancreatic dysfunction and β-cell stress within a broader gut-liver axis context. We further discuss the systemic propagation of MPs/NPs-induced dysbiosis along multi-organ axes, including gut-lung and gut-brain interactions. Despite robust preclinical data, human evidence remains limited due to methodological heterogeneity and the lack of standardized biomarkers. This review underscores critical knowledge gaps and emphasizes the need for integrative, translational approaches to clarify long-term health risks and inform regulatory strategies within the environmental exposome framework.
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This review summarizes what scientists know about how micro- and nanoplastics affect the liver, which is one of the first organs exposed because it processes everything absorbed from the gut. The particles trigger oxidative stress, disrupt energy metabolism, cause cell death, and promote inflammation, and may contribute to conditions like fatty liver disease and liver fibrosis. The paper also highlights how plastics can disturb the gut microbiome, which communicates with the liver through the gut-liver axis and may amplify liver damage.
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This review describes how microplastics can damage the liver through the gut-liver axis: they first disrupt the gut's protective barrier and beneficial bacteria, allowing harmful substances to leak through the weakened intestinal wall into the bloodstream and travel to the liver. Once there, these substances cause inflammation, metabolic problems, and oxidative stress, offering a new explanation for how microplastic exposure could lead to liver disease.
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This review examines how nanoplastics, particles smaller than 100 nanometers, accumulate in and damage the liver. Researchers found that nanoplastics enter the body through the respiratory and digestive systems, reach the liver via the bloodstream, and can disrupt the gut-liver axis and gut microbiome. The evidence suggests that liver damage from nanoplastics may trigger cascading effects on other organs, highlighting the need for further research on these less visible pollutants.
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This review examines emerging evidence linking micro- and nanoplastic exposure to liver disease, including metabolic dysfunction-associated liver disease, cirrhosis, and liver cancer. Researchers found that these particles may contribute to liver damage through oxidative stress, inflammation, and disruption of metabolic pathways. The study highlights the need for further research into how environmental plastic contamination may be influencing the rising rates of liver disease worldwide.
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Researchers reviewed emerging evidence that microplastics and nanoplastics accumulate in human liver tissue at increasing concentrations over the past decade, trigger oxidative stress, fibrogenesis, and inflammation in cell and animal models, and may carry microbial pathogens and endocrine-disrupting chemicals, introducing the concept of plastic-induced liver injury as a new focus for environmental hepatology.
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