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61,005 resultsShowing papers similar to Reversibility of Renal Fibrosis Induced by Exposure to Polystyrene Nanoplastics: The Dual Role of Lysosomes
ClearReversibilityofRenal Fibrosis Induced by Exposureto Polystyrene Nanoplastics: The Dual Role of Lysosomes
This mouse study investigated whether kidney fibrosis caused by low-level polystyrene nanoplastics (100 nm and 500 nm) is reversible, finding that 100 nm particles caused more severe fibrosis and that lysosomes played a dual role — initially impairing autophagy flux to promote fibrosis, then recovering to facilitate partial reversal after exposure ended.
The size-dependence and reversibility of polystyrene nanoplastics-induced lipid accumulation in mice: Possible roles of lysosomes
This mouse study found that smaller nanoplastics (100 nm) cause more fat buildup in the liver than larger ones (500 nm), showing that size matters when it comes to health effects. Encouragingly, the liver damage was reversible after the mice stopped being exposed, suggesting the body can recover once nanoplastic intake is reduced. The damage appears to work by disrupting the cell's waste-recycling system (lysosomes).
Effects of nano- and microplastics on kidney: Physicochemical properties, bioaccumulation, oxidative stress and immunoreaction
Researchers exposed mice to polystyrene nano- and microplastics of varying sizes and tracked their accumulation and effects in the kidneys. They found that the particles changed their physical properties during digestion, accumulated in kidney tissue, and caused oxidative stress and immune responses. The study suggests that plastic particle size plays an important role in determining the extent of kidney-related harm.
Polystyrene microplastics facilitate renal fibrosis through accelerating tubular epithelial cell senescence
Mice exposed to polystyrene microplastics at doses relevant to human exposure developed kidney inflammation and scarring (fibrosis) within 28 days. The microplastics caused kidney tube cells to age prematurely, triggering a chain reaction that activated scar-forming cells through a specific signaling pathway. This study provides evidence that microplastic exposure could contribute to chronic kidney damage in people.
Chronic exposure to polystyrene microplastics induces renal fibrosis via ferroptosis
Mice exposed to polystyrene microplastics in their drinking water for six months developed kidney scarring (fibrosis) driven by a type of cell death called ferroptosis. The microplastics triggered iron-dependent damage in kidney cells, which then released signals causing surrounding tissue to scar over. This long-term study reveals a new mechanism by which chronic microplastic exposure could lead to progressive kidney disease in humans.
Compromised Autophagic Effect of Polystyrene Nanoplastics Mediated by Protein Corona Was Recovered after Lysosomal Degradation of Corona
Researchers discovered that when polystyrene nanoplastics enter biological environments, proteins coat their surface forming a protective corona that initially reduces their toxic effects on cells. However, once cells internalize the particles and break down the protein layer in lysosomes, the original toxicity returns, including blocked autophagy and lysosomal damage. The study reveals that protein coronas temporarily mask nanoplastic toxicity rather than permanently neutralizing it.
Polystyrene nanoparticles with different particle sizes cause autophagy by ROS/ERS/FOXO1 axis in the Cyprinus carpio kidney affecting immunological function
Researchers exposed common carp to polystyrene nanoparticles of three different sizes and found that all sizes caused kidney damage by triggering oxidative stress, endoplasmic reticulum stress, and abnormal autophagy. Smaller nanoparticles generally produced more severe effects, disrupting immune-related gene expression and cellular cleanup processes in the kidney. The study suggests that nanoplastic size matters significantly for toxicity, with the tiniest particles posing the greatest risk to fish organ health.
Screening for polystyrene nanoparticle toxicity on kidneys of adult male albino rats using histopathological, biochemical, and molecular examination results
Researchers found that oral exposure to polystyrene nanoparticles caused significant kidney damage in rats, including oxidative stress, impaired renal function, and tissue alterations that worsened with increasing dose, demonstrating their nephrotoxic potential.
Toxicological effects and mechanisms of renal injury induced by inhalation exposure to airborne nanoplastics
Researchers studied what happens to mouse kidneys after breathing in airborne polystyrene nanoplastics and found the particles accumulated in kidney tissue after entering through the lungs. The nanoplastics activated stress and inflammation pathways that led to kidney cell damage and death. Testing on lab-grown human kidney organoids showed they were even more sensitive to nanoplastic exposure than standard cell lines, suggesting developing kidneys in embryos could be particularly vulnerable.
Exploring the Mechanismof Kidney Injury in Mice Inducedby High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Throughthe Kidney-Gut Axis
This mouse study found that combining a high-fat diet with polystyrene nanoplastic exposure (100 nm, 25 mg/kg/day) worsened kidney toxicity beyond high-fat diet alone, with the combination disrupting lipid metabolism via tryptophan and glycerophospholipid pathways and exacerbating gut microbiota dysbiosis through the kidney-gut axis.
Polystyrene nanoplastics target lysosomes interfering with lipid metabolism through the PPAR system and affecting macrophage functionalization
Researchers examined how polystyrene nanoplastics affect lysosomal function and lipid metabolism in macrophages through the PPAR signaling system. The study suggests that nanoplastics can interfere with cellular lipid processing by targeting lysosomes, which may affect immune cell function.
Hepatotoxic mechanisms of functionalized nanopolystyrene: decoding the role of ionic surface groups
Researchers exposed mice to polystyrene nanoplastics with different surface charges via drinking water, finding that charged particles accumulate in liver sinusoids and induce hepatocyte ferroptosis through an endoplasmic reticulum stress cascade, while neutral particles cause endothelial cell senescence through lysosomal dysfunction.
The Kidney-Related Effects of Polystyrene Microplastics on Human Kidney Proximal Tubular Epithelial Cells HK-2 and Male C57BL/6 Mice
This study found that polystyrene microplastics caused damage to human kidney cells in the lab and accumulated in the kidneys of mice. The microplastics triggered mitochondrial dysfunction, inflammation, and a cellular stress response called autophagy in kidney tissue. These results suggest that long-term microplastic exposure could be a risk factor for kidney disease.
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.
Hazard Assessment of Polystyrene Nanoplastics in Primary Human Nasal Epithelial Cells, Focusing on the Autophagic Effects
Researchers exposed primary human nasal epithelial cells to polystyrene nanoplastics of two sizes and found that the smaller particles caused more significant cellular changes, including activation of autophagy pathways. The nanoplastics triggered oxidative stress and altered cell processes related to waste recycling within cells. The study highlights the potential health risks of inhaling airborne nanoplastics, an exposure route that remains understudied.
Effects of Orally Ingested Microplastics on the Structure and Function of the Kidneys
This study reviewed the structural and functional effects of orally ingested microplastics on kidney tissue, synthesizing experimental evidence from animal and in vitro studies. Microplastic exposure was consistently associated with kidney histopathology including inflammation and fibrosis, with particle size, shape, and polymer type influencing the severity of renal damage.
Polystyrene nanoplastics induce lipophagy via the AMPK/ULK1 pathway and block lipophagic flux leading to lipid accumulation in hepatocytes
Polystyrene nanoplastics caused fat to accumulate in human liver cells by disrupting the normal fat-breakdown process called lipophagy. The nanoplastics triggered the cells to start digesting fat droplets but then blocked the final cleanup step by damaging the cell's recycling centers (lysosomes), leaving excess fat trapped inside. This newly identified mechanism helps explain how nanoplastic exposure could contribute to fatty liver disease.
New Sight of Renal Toxicity Caused by UV‐Aged Polystyrene Nanoplastics: Induced Ferroptosis via Adsorption of Transferrin
Researchers discovered that polystyrene nanoplastics aged by sunlight caused more severe kidney damage in mice than fresh nanoplastics, triggering a type of cell death called ferroptosis. The sun-aged particles grabbed onto a blood protein called transferrin, which carries iron into cells, causing iron overload and cell damage in kidney tissue. This is concerning because most nanoplastics in the real world have been weathered by UV light, meaning they may be more harmful to human kidneys than laboratory studies using fresh plastics suggest.
Autophagic response of intestinal epithelial cells exposed to polystyrene nanoplastics
Researchers found that polystyrene nanoplastics accumulate in the cytoplasm of intestinal epithelial cells, impairing autophagic flux and triggering an autophagic stress response confirmed in both cell and animal models.
Nanoplastic toxicity and uptake in kidney cells: differential effects of concentration, particle size, and polymer type
Researchers exposed human kidney proximal tubule cells to nanoplastics of different polymer types, sizes, and concentrations to assess short-term toxic effects. They found that polystyrene and PMMA nanoparticles were readily internalized by kidney cells and caused concentration-dependent reductions in cell viability and changes in cell cycle distribution. The study suggests that nanoplastics can directly affect kidney cell function, with toxicity varying by polymer type and particle size.
PS-MPs promotes the progression of inflammation and fibrosis in diabetic nephropathy through NLRP3/Caspase-1 and TGF-β1/Smad2/3 signaling pathways.
In a mouse model of diabetic nephropathy, polystyrene microplastic exposure worsened kidney inflammation and fibrosis by activating the NLRP3/Caspase-1 and TGF-beta1/Smad2/3 signaling pathways, suggesting microplastics may accelerate progression of this common diabetic complication.
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.
Stress Response of Mouse Embryonic Fibroblasts Exposed to Polystyrene Nanoplastics
Mouse embryonic fibroblasts exposed to polystyrene nanoplastics internalized particles via endocytosis without losing viability, but showed activation of antioxidant and autophagic stress pathways, suggesting subcellular dysfunction even in the absence of cell death.
Nanoplastic toxicity and uptake in kidney cells: differential effects of concentration, particle size, and polymer type
Human proximal tubule kidney cells were exposed to carboxylated polystyrene and PMMA nanoplastics of different sizes for 24 hours, revealing that cytotoxicity, cellular uptake, and oxidative stress were strongly dependent on particle concentration, size, and polymer type.