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Micro- and nanoplastics induce hepatic injury through organelle stress and fibrotic signaling: mechanisms and therapeutic opportunities
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This review pulls together existing research showing that tiny plastic particles we ingest (from food, water, and packaging) can build up in the liver and damage it from the inside, stressing the cell's internal "power plants" and "recycling centers," triggering inflammation, and eventually causing scarring (fibrosis). This matters because it suggests everyday plastic exposure could contribute to chronic liver disease over time, and the paper points to potential treatments, like antioxidants or therapies targeting gut health, that scientists are exploring to counter this damage.
Micro- and nanoplastics (MNPs) have emerged as widespread environmental contaminants and are increasingly being detected in human tissues, including the liver. As the primary organ responsible for detoxification and metabolic regulation, the liver is particularly vulnerable to the accumulation of these particles following gastrointestinal absorption and systemic distribution. Growing evidence suggests that MNPs are not biologically inert but actively interfere with intracellular homeostasis, leading to progressive hepatic injury. This review summarizes current evidence on the mechanisms by which MNPs contribute to liver dysfunction, with a particular focus on organelle stress and fibrotic signaling. Following cellular uptake, MNPs accumulate within hepatocytes and Kupffer cells, where they disrupt mitochondrial function, induce excessive reactive oxygen species production, trigger endoplasmic reticulum stress, and impair lysosomal degradation and autophagic clearance. These interconnected disturbances form an organelle stress network that promotes persistent cellular dysfunction. The resulting oxidative and proteostatic stress activates inflammatory pathways, including NF-κB and the NLRP3 inflammasome, leading to sustained production of pro-inflammatory cytokines and amplification of hepatic injury. Chronic inflammation and unresolved intracellular stress subsequently drive activation of hepatic stellate cells through profibrotic mediators such as transforming growth factor-β (TGF-β) and Smad signaling, resulting in extracellular matrix deposition and progressive fibrotic remodeling. We propose an integrated framework linking MNP physicochemical properties, hepatic accumulation, organelle dysfunction, inflammatory amplification, and fibrosis development. In addition, emerging therapeutic strategies targeting oxidative stress, inflammasome activation, autophagy dysfunction, and the gut–liver axis are discussed. The current evidence supports the view that MNPs function as persistent intracellular stressors capable of initiating and sustaining pathways associated with chronic liver disease. A better understanding of these mechanisms will be essential for risk assessment and for the development of effective preventive and therapeutic interventions.
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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.
Micro- and Nanoplastics as Emerging Drivers of Liver Injury: Exposure, Evidence, and Mechanisms
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This review pulls together current research on tiny plastic particles (microplastics and nanoplastics) that we ingest or breathe in, showing they can travel through the body and accumulate in the liver. Lab studies suggest these particles may trigger inflammation, stress cells out, and disrupt normal liver function in ways that could contribute to fatty liver disease and scarring over time. That said, most of this evidence comes from animal and cell studies so far—scientists still need more direct human data to know exactly how much this matters for our health, but it's a good reason to be mindful of plastic exposure in food and water.
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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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