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Exposure to microplastics and liver oncogenesis: A comprehensive review on molecular mechanisms and pathogenic pathways
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Researchers reviewed mechanisms by which microplastic exposure may promote liver cancer, identifying oxidative stress, mitochondrial dysfunction, inflammatory signaling, and epigenetic disruption as key pathways, while noting that microplastics can also carry heavy metals and organic pollutants that synergistically amplify hepatotoxic and carcinogenic risk.
Microplastics have become a serious environmental pollutant that enter different ecosystems and eventually the human body through direct exposure to the environment. This infiltration is a major health risk, especially for the liver, which is a primary metabolic organ highly sensitive to the harmful effects of microplastics. There are many ways that these particles can cause liver damage, such as disrupting metabolism, inducing oxidative stress, causing mitochondrial dysfunction, causing inflammation, changing gene expression, and activating abnormal signaling pathways. Even in the absence of hepatic fibrosis or cirrhosis, the carcinogenic potential of microplastics may exert its effects through different pathways. In addition, microplastics can act as efficient vectors for the transport of heavy metals, organic pollutants, and pathogenic microorganisms, thereby synergistically amplifying the toxic effects of these agents and increasing health risks. The complex interactions between microplastics and various pathological processes underscore their critical role in the development of hepatocellular carcinoma. Future research endeavors should focus on elucidating the long-term health impacts of microplastic exposure to devise effective public health policies and preventive strategies.
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Microplastics and nanoplastics: Emerging drivers of hepatic pathogenesis and metabolic dysfunction
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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.
Hepatotoxic Mechanisms of Micro- and Nanoplastics in Animal Models: A Scoping Review with Human Health Implications
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This scoping review examines hepatotoxic mechanisms of micro- and nanoplastics in animal models, identifying oxidative stress, inflammation, lipid peroxidation, and epigenetic alterations as the primary pathways through which plastic particles damage liver tissue.
The mechanistic nexus between microplastics and chronic liver disease: A review of current evidence
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Researchers reviewed the mechanisms by which microplastics accumulate in liver tissue and worsen chronic liver disease, finding that MPs activate cell death pathways, trigger oxidative stress and inflammation, promote fibrosis, and disrupt metabolic and microbial regulation — and can amplify damage from co-occurring hepatotoxic substances.
Microplastics, nanoplastics and liver disease: an emerging health concern?
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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.
Long-Term Exposure to Microplastics Promotes Early-Stage Hepatocarcinogenesis Induced by Diethylnitrosamine in Rats by Modulation of Their Gut Microbiota
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Using a long-term mouse exposure model, researchers found that chronic microplastic ingestion promoted early-stage liver cancer development through oxidative stress, inflammation, and epigenetic alterations, providing mechanistic evidence for a microplastics-hepatocarcinogenesis link.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.