We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene Nanoplastics Exacerbate CCl4-Induced Liver Fibrosis by Aggravating Stretch-Induced Mechanical Stress in Hepatic Stellate Cells
AI summary Read the abstract
Researchers found that chronic exposure to polystyrene nanoplastics worsens chemical-induced liver fibrosis in mice by directly activating hepatic stellate cells through a stretch-induced mechanical stress pathway involving the TGF-β receptor, independent of macrophage-mediated inflammation.
Although studies on the potential hepatotoxicity of nanoplastic depositions are being conducted, there remains a lack of research on the association between nanoplastic depositions and chronic liver disease.Therefore, this research aimed to explore the influence of polystyrene nanoparticles (PS-NPs) on the progression of liver fibrosis and the mechanisms involved in the hepatic stellate cells (HSCs) activation.Chronic exposure to PS-NPs aggravated CCl-induced liver fibrosis, as evidenced by enhanced collagen accumulation and elevated -smooth muscle actin (-SMA) expression.Most PS-NPs were accumulated in non-parenchymal liver cells, with Kupffer cells exhibiting the highest uptake.This accumulation was associated with enhanced recruitment of CD68-positive macrophages.However, PS-NPs were not associated with TGF- expression in CD68-positive cells.Additionally, CD68positive cells treated with PS-NPs did not affect -SMA expression in HSCs.Further in vitro experiments revealed that -SMA and pSmad2/3 were directly promoted by PS-NPs in both LX-2 HSCs and primary isolated HSCs, indicating a direct stimulatory effect on HSC activation.PS-NPs enhanced pTGFBR1 expression of HSCs by promoting stretch-induced mechanical stress, suggesting a novel pathway through which nanoplastics may exacerbate fibrogenesis.Our findings provide the first evidence that PS-NPs, as xenobiotic particles, can directly promote HSC activation and exacerbate liver fibrosis, indicating potential health risks associated with chronic nanoplastic exposure.
More Papers Like This
Polystyrene nanoplastics exacerbate dibutyl phthalate-induced liver fibrosis through PDGFRα-dependent hepatic stellate cell activation
AI summary Read the abstract
Researchers found that polystyrene nanoplastics worsen liver fibrosis caused by dibutyl phthalate, a common plasticizer, through activation of hepatic stellate cells via the PDGFRalpha signaling pathway. The study suggests that nanoplastics act as environmental carriers that facilitate cellular uptake of harmful plasticizers, amplifying their toxic effects on liver tissue.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
AI summary Read the abstract
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.
Nanoplastics remodel the extracellular matrix mechanical microenvironment to activate hepatic stellate cells
AI summary Read the abstract
Polystyrene nanoplastics — especially carboxylated PS-COOH particles — were retained in collagen hydrolysate matrices mimicking the liver's space of Disse, increasing matrix viscosity and indirectly activating hepatic stellate cells through mechanical remodeling of the extracellular matrix. This is significant for microplastic health research because it identifies a novel, indirect mechanism by which nanoplastics could initiate liver fibrosis without requiring direct cytotoxicity.
Polystyrene microplastics and hepatic fibrosis-related indices in type 2 diabetes: a cross-sectional analysis with experimental validation
AI summary Read the abstract
Researchers found that polystyrene microplastics detected in blood were the polymer most consistently linked to elevated liver fibrosis markers in type 2 diabetic patients, and confirmed in diabetic mice that PS-MPs worsen hepatic steatosis and fibrosis by activating the NLRP3 inflammasome and TGF-β1/Smad signaling pathways.
Accumulation of polystyrene microplastics induces liver fibrosis by activating cGAS/STING pathway
AI summary Read the abstract
Researchers found that tiny polystyrene microplastics (0.1 micrometers) can enter liver cells and cause DNA damage that triggers a chain reaction leading to liver scarring, known as fibrosis. The microplastics activated a specific immune signaling pathway called cGAS/STING, which caused inflammation that progressively damaged liver tissue even at low concentrations. This study reveals a specific mechanism by which long-term microplastic exposure could lead to serious liver disease in humans.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.