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61,005 resultsShowing papers similar to Assessment of cancer-related signaling pathways in responses to polystyrene nanoplastics via a kidney-testis microfluidic platform (KTP)
ClearPolystyrene nanoplastics induce apoptosis of human kidney proximal tubular epithelial cells via oxidative stress and MAPK signaling pathways
Researchers found that polystyrene nanoplastics cause programmed cell death in human kidney tubular cells through oxidative stress and activation of the MAPK signaling pathway. The toxic effects were dependent on both the size and dose of the nanoplastics, with smaller particles causing more damage. The study identifies specific molecular mechanisms by which nanoplastics may contribute to kidney cell injury.
Uptake and effects of polystyrene nanoplastics in comparison to non-plastic silica nanoparticles on small intestine cells (IPEC-J2)
Researchers exposed small intestine cells to 100 nm polystyrene nanoplastics and found the particles were taken up by cells and significantly altered the TP53 and NOTCH signaling pathways — key regulators of cell survival and growth — raising concerns about how nanoplastics ingested through food might affect gut cell function.
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.
Polystyrene Microplastics Exposure Aggravates Clear Cell Renal Cell Carcinoma Progression via the NF‐κB and TGF‐β Signaling Pathways
Researchers detected polystyrene microplastics in clear cell renal cell carcinoma tissue samples and showed in cell culture and animal models that microplastic exposure aggravated cancer progression by activating NF-κB and TGF-β signaling pathways that promote tumor growth and spread.
Polystyrene nanoplastics induce profound metabolic shift in human cells as revealed by integrated proteomic and metabolomic analysis
Researchers used integrated proteomic and metabolomic analysis to study how polystyrene nanoplastics affect human kidney and liver cell lines. The study quantified changes in thousands of proteins and hundreds of metabolites, revealing that nanoplastic exposure induced a profound metabolic shift in human cells. Evidence indicates that nanoplastics can be internalized by human cells and trigger significant biological changes at the molecular level.
Comparative evaluation of molecular mechanisms triggered by differently functionalized polystyrene nanoplastics in human colon cell lines
Researchers compared the molecular responses triggered by polystyrene nanoplastics with different surface chemical groups in human colon cell lines. The study investigated how the specific functionalization of nanoplastic surfaces influences the cellular and molecular pathways activated upon exposure in human intestinal tissue.
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.
Polystyrene microplastic-induced extracellular vesicles cause kidney-related effects in the crosstalk between tubular cells and fibroblasts
Researchers found that polystyrene microplastics cause kidney tubule cells to release tiny signaling packages (extracellular vesicles) that trigger stress responses and scarring in neighboring kidney cells. This cell-to-cell communication pathway spread the damage beyond the cells directly exposed to the microplastics. The findings suggest a mechanism by which microplastic exposure could contribute to kidney fibrosis and long-term kidney damage in humans.
Polystyrene microplastics disrupt kidney organoid development via oxidative stress and Bcl-2/Bax/caspase pathway
Researchers used lab-grown kidney organoids made from human stem cells to study how polystyrene microplastics affect kidney development. The microplastics triggered oxidative stress and activated cell death pathways, disrupting the formation of key kidney structures. This study provides direct evidence that microplastic exposure could interfere with human organ development, which is especially concerning for fetuses and young children.
Polystyrene Nanoplastics at an Environmentally Relevant Concentration Promote Ovarian Cancer Progression via CDK4/6-Dependent Signaling
Researchers demonstrated that polystyrene nanoplastics at concentrations as low as 20 μg/mL—consistent with environmental exposure levels—significantly promoted ovarian cancer cell proliferation through CDK4/6 signaling, providing evidence of a potential carcinogenic risk from nanoplastic exposure.
Investigating polystyrene nanoplastics-induced reproductive toxicity in vitro: Focus on Nrf2-PKM2-autophagy signaling pathway
This lab study investigated how polystyrene nanoplastics damage male reproductive cells, finding they triggered autophagy (cellular self-digestion) and disrupted key proteins in a signaling pathway important for sperm cell survival. The findings suggest nanoplastics could impair male fertility by causing programmed cell death in testicular cells. This adds to growing evidence that plastic nanoparticles can harm reproductive health.
Comparative analysis of reproductive toxicity of polystyrene‐nanoplastics and polystyrene‐microplastics in rat Sertoli cells
This comparative study found that polystyrene nanoplastics cause greater toxicity to Sertoli cells than microplastics due to cellular internalization, disrupting blood-testis barrier integrity via oxidative stress and apoptosis, while microplastics primarily triggered extracellular inflammation.
The nephrotoxic potential of polystyrene microplastics at realistic environmental concentrations
Researchers tested polystyrene microplastics on human kidney cells at concentrations reflecting real-world environmental levels. They found that the particles attached to and were engulfed by the cells, triggering oxidative stress and inflammatory responses that reduced cell survival. The findings suggest that even realistic low-level microplastic exposure may pose risks to kidney health.
Effects of Polystyrene Microplastics on Human Kidney and Liver Cell Morphology, Cellular Proliferation, and Metabolism
Researchers exposed human kidney and liver cells to polystyrene microplastics of different sizes and concentrations to assess their effects on cell health. They found that microplastics altered cell shape, reduced proliferation, and disrupted cellular metabolism, with smaller particles generally causing more damage. The findings suggest that microplastics reaching internal organs could have measurable effects at the cellular level.
Polystyrene microplastics induce apoptosis in chicken testis via crosstalk between NF-κB and Nrf2 pathways
Researchers found that polystyrene microplastics caused testicular damage in chickens through crosstalk between inflammatory and antioxidant defense pathways. Exposure to microplastics through drinking water disrupted the blood-testis barrier, triggered oxidative stress by inhibiting the Nrf2 pathway, activated inflammatory signaling through NF-kB, and ultimately induced cell death in testicular tissue.
Polystyrene Nanoplasticsat an Environmentally RelevantConcentration Promote Ovarian Cancer Progression via CDK4/6-DependentSignaling
Researchers found that polystyrene nanoplastics at environmentally relevant concentrations (20 μg/mL) promoted ovarian cancer cell proliferation through CDK4/6-dependent signaling, representing the first evidence that environmentally relevant nanoplastic levels may drive ovarian cancer progression.
Issue Information‐ToC
This brief notice indicates a paper in the journal issue that examines how polystyrene nanoplastics worsen inflammation-triggered cell death (apoptosis) in mouse kidney cells exposed to bacterial toxins. The interaction between nanoplastics and inflammatory signals may amplify kidney damage beyond what either stressor alone would cause.
Polystyrene nanoplastics and lung cancer: Insights from network toxicology and mechanistic in vitro studies
Network toxicology analysis identified 189 potential molecular targets linking polystyrene nanoplastic exposure to lung cancer pathways, and in vitro experiments confirmed that nanoplastics promote lung cancer cell proliferation and resistance to apoptosis via PI3K/AKT signaling.
The crosstalk between M1 macrophage polarization and energy metabolism disorder contributes to polystyrene nanoplastics-triggered testicular inflammation
Researchers investigated how polystyrene nanoplastics cause testicular inflammation in mice by studying the interplay between immune cell behavior and energy metabolism. They found that nanoplastics triggered a pro-inflammatory immune response involving M1 macrophage activation, disrupted cellular energy processes, and caused testicular tissue damage. The study reveals a specific biological mechanism by which nanoplastic exposure may impair male reproductive health.
Cytotoxic effect of polystyrene nanoplastics in human umbilical vein endothelial cells (HUVECs) and normal rat kidney cells (NRK52E)
Researchers tested how polystyrene nanoplastics affect human blood vessel cells and rat kidney cells in the lab. They found that nanoplastic exposure caused oxidative stress and reduced cell survival in both cell types, with effects increasing at higher concentrations. The study adds to growing evidence that nanoplastics can damage mammalian cells, though the implications for whole-body health require further investigation.
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.
Polystyrene nanoplastics affect transcriptomic and epigenomic signatures of human fibroblasts and derived induced pluripotent stem cells: Implications for human health
Researchers found that polystyrene nanoplastics altered transcriptomic and epigenomic signatures in human fibroblasts and derived induced pluripotent stem cells, demonstrating that plastic particle exposure can cause lasting molecular changes with potential implications for human health.
Long-term exposure to nanoplastics alters molecular and functional traits related to the carcinogenic process
Researchers exposed cells to polystyrene nanoplastics for six months and found that long-term exposure activated multiple molecular markers associated with cancer development, including enhanced cell migration, invasion potential, and ability to grow independently. The study suggests that chronic nanoplastic exposure may pose a carcinogenic risk, though further research is needed to confirm these findings in living organisms.
Oral exposure to polystyrene nanoplastics altered the hypothalamic–pituitary–testicular axis role in hormonal regulation, inducing reproductive toxicity in albino rats
This study found that oral exposure to polystyrene nanoplastics disrupted the hormone signaling pathway between the brain and testes in male rats, leading to reproductive damage. The nanoplastics interfered with the hormones that regulate sperm production and testicular function. These findings add to growing evidence that nanoplastic exposure through food and water could be a contributing factor to declining male fertility.