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20 resultsShowing papers similar to Nanoplastic propels diet-induced NAFL to NASH via ER-mitochondrial tether-controlled redox switch
ClearNanoplastic Exposure at Environmental Concentrations Disrupts Hepatic Lipid Metabolism through Oxidative Stress Induction and Endoplasmic Reticulum Homeostasis Perturbation
A study in fish found that nanoplastics at environmentally realistic concentrations accumulated in the liver and disrupted fat metabolism, causing a condition similar to fatty liver disease. Smaller nanoplastics (100 nanometers) caused more severe damage than larger microplastics by disrupting protein processing in cells and triggering oxidative stress. These findings raise concerns that nanoplastics in the environment could affect liver health in fish and potentially in humans who consume contaminated seafood.
Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease
This review examines how environmental toxicants, including micro and nanoplastics, target fat tissue and contribute to metabolic diseases like obesity, diabetes, and fatty liver disease. These pollutants disrupt mitochondria (the energy-producing parts of cells) and trigger a cycle of oxidative stress and inflammation that damages both fat tissue and the liver. The findings suggest that microplastic exposure could be one of several environmental factors contributing to the rising rates of metabolic disease worldwide.
Chronic Nanoplastic Exposure Promotes the Development and Progression of Metabolic Dysfunction‐Associated Steatotic Liver Disease
This study found that chronic exposure to nanoplastics promotes the development and worsening of metabolic dysfunction-associated steatotic liver disease (formerly known as fatty liver disease). Nanoplastics appear to increase vulnerability to liver disease progression. The finding is concerning because fatty liver disease is already widespread, and everyday nanoplastic exposure through food and water could be making it worse.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.
Microplastics and nanoplastics: Emerging drivers of hepatic pathogenesis and metabolic dysfunction
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
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.
Chronic Nanoplastic Exposure as a Novel Risk Amplifier for MASLD Progression
This study examines the potential for chronic nanoplastic exposure to amplify the progression of metabolic dysfunction-associated steatotic liver disease. The research explores how persistent nanoplastic exposure may act as a novel risk factor that worsens liver disease outcomes. The findings highlight growing concern about the intersection of plastic pollution and metabolic health conditions.
Impact of microplastics and nanoplastics on liver health: Current understanding and future research directions
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.
Microplastics in metabolic dysfunction-associated steatotic liver disease: An emerging threat to liver health
This review examined emerging evidence linking microplastic exposure to the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD). The authors found that microplastics detected in liver tissue can exacerbate hepatic inflammation, lipid accumulation, and oxidative stress through multiple mechanisms, adding a novel environmental risk factor to MASLD pathogenesis.
Are Ingested or Inhaled Microplastics Involved in Nonalcoholic Fatty Liver Disease?
This review explored the potential connection between microplastic exposure through ingestion and inhalation and nonalcoholic fatty liver disease, which has become a leading cause of chronic liver injury. The study discusses how dietary and environmental microplastic exposure could potentially influence liver health through mechanisms including inflammation and endocrine disruption, though further research is needed to establish definitive links.
The nexus of environmental endocrine-disrupting chemical exposure and metabolic dysfunction-associated steatotic liver disease: An emerging public health challenge
This review examines evidence that chronic low-dose exposure to endocrine-disrupting chemicals, including micro- and nanoplastics, may be an underappreciated factor driving the global rise of metabolic liver disease. Researchers found that these pollutants can promote liver fat accumulation, inflammation, and scarring by disrupting hormone signaling, gut health, and mitochondrial function. The study suggests that environmental chemical exposures should be considered alongside diet and lifestyle when assessing liver disease risk.
Oxidative stress-activated Nrf2 remitted polystyrene nanoplastic-induced mitochondrial damage and inflammatory response in HepG2 cells
Researchers discovered that polystyrene nanoplastics damage human liver cells by causing oxidative stress and mitochondrial damage, but the cells activate a protective pathway called Nrf2 to fight back. When the Nrf2 defense was blocked, the damage from nanoplastics became significantly worse, confirming its protective role. This study helps explain how the liver tries to defend itself against nanoplastic toxicity, and suggests that people with weaker antioxidant defenses may be more vulnerable to liver damage from plastic exposure.
Molecular Landscape Remodeling Unravels the Cross-Links of Microplastics-Induced Lipidomic Fluctuations, Nutrient Disorders and Energy Disarrangements
Researchers fed mice polypropylene microplastics chronically and used lipidomics and transcriptomics to show that microplastics accumulated in the liver and disrupted lipid metabolism, cholesterol homeostasis, and redox balance, with high doses causing fibrotic liver changes.
ROS and DRP1 interactions accelerate the mitochondrial injury induced by polystyrene nanoplastics in human liver HepG2 cells
This study found that polystyrene nanoplastics damage human liver cells by triggering harmful interactions between reactive oxygen species (ROS) and a protein called DRP1 that controls mitochondria. The nanoplastics caused mitochondria to break apart, leading to cell injury and death. This research helps explain how microplastic exposure could contribute to liver damage in humans at the cellular level.
Single-cell transcriptome analysis of liver immune microenvironment changes induced by microplastics in mice with non-alcoholic fatty liver
Using advanced single-cell analysis, researchers showed that microplastics worsened non-alcoholic fatty liver disease in mice fed a high-fat diet by changing how immune cells behaved in the liver. Microplastic exposure amplified inflammatory responses and altered the communication between different liver cell types. This study is important because it reveals specific immune mechanisms by which microplastics could worsen liver disease, a condition already affecting roughly one in four adults worldwide.
Polystyrene Nanoplastics Exacerbate HFD-induced MASLD by Reducing Cathepsin Activity and Triggering Large Vacuole Formation via Impaired Lysosomal Acidification
Researchers found that polystyrene nanoplastics, when combined with a high-fat diet in mice, significantly worsened fatty liver disease symptoms compared to either factor alone. The nanoplastics impaired the function of lysosomes, the cell's recycling centers, by preventing proper acidification and reducing enzyme activity. The study suggests that nanoplastic exposure could amplify diet-related liver problems by interfering with how cells process and break down fats.
Exposure to submicroplastics promotes the progression of nonalcoholic fatty liver disease in ApoE-deficient mice
Researchers found that exposing mice to submicron-sized polystyrene plastics in their drinking water for 12 weeks accelerated the progression of nonalcoholic fatty liver disease. The tiny plastic particles accumulated in the liver, worsened fat buildup, increased inflammation, and disrupted cholesterol metabolism. This study suggests that people who already have risk factors for liver disease may be especially vulnerable to health effects from microplastic exposure.
Exposure to microplastics and liver oncogenesis: A comprehensive review on molecular mechanisms and pathogenic pathways
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.
Nano‐plastics disrupt systemic metabolism by remodeling the bile acid–microbiota axis and driving hepatic–intestinal dysfunction
Mice were exposed to polyethylene terephthalate nanoparticles, and researchers used histopathology, metabolomics, and metagenomics to track downstream effects. Nanoplastic ingestion caused severe metabolic disruption—including weight loss, organ atrophy, and liver-intestinal dysfunction—by remodeling the bile acid–gut microbiota axis.
A computational framework for multi-scale data fusion in assessing the associations between micro- and nanoplastics and human hepatotoxicity
Researchers developed a computational toxicology framework integrating multi-source data and network analysis to map associations between micro- and nanoplastics and hepatotoxicity, identifying key molecular pathways through which MNPs may damage the liver, offering a scalable alternative to traditional in vivo testing.