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20 resultsShowing papers similar to Polystyrene Microplastics Exposure Aggravates Clear Cell Renal Cell Carcinoma Progression via the NF‐κB and TGF‐β Signaling Pathways
ClearMultimodal detection and analysis of microplastics in human clear cell renal cell carcinoma
Researchers used multiple detection methods to analyze microplastics in tumor and normal kidney tissue from patients with clear cell renal cell carcinoma. They found that tumor tissues contained significantly higher levels of total microplastics, particularly polyethylene and PVC, compared to surrounding normal tissue. Gene expression analysis revealed that patients with higher microplastic levels showed activation of signaling pathways associated with tumor progression, suggesting a potential link worth further investigation.
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.
Assessment of cancer-related signaling pathways in responses to polystyrene nanoplastics via a kidney-testis microfluidic platform (KTP)
Researchers developed a kidney-testis microfluidic platform to assess cancer-related signaling pathway responses to polystyrene nanoplastics. The study found that nanoplastic exposure activated cancer-associated signaling pathways in both kidney and testis tissue models, providing new insights into the potential molecular mechanisms through which nanoplastics may affect organ health.
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 polystyrene microplastics exposure promotes lung adenocarcinoma metastasis through EREG-regulated phosphorylation-dependent NF-κB activation
Researchers found that chronic exposure to polystyrene microplastics significantly enhanced the migration, invasion, and proliferation of lung adenocarcinoma cells in laboratory and animal models. The microplastics activated a protein called EREG that triggered NF-kB signaling, a pathway associated with tumor progression and metastasis. The study also found that high EREG expression correlated with worse clinical outcomes in lung cancer patients, suggesting a molecular mechanism by which microplastic exposure could promote cancer spread.
Identification and analysis of microplastics in para-tumor and tumor of human prostate
Researchers detected microplastics in both tumor and surrounding tissue from 22 prostate cancer patients, with polystyrene found exclusively in tumor tissue. Larger microplastic particles were more common in tumors, and higher microplastic levels correlated with more advanced cancer stages, suggesting a potential link between microplastic accumulation and prostate cancer progression.
Polystyrene microplastics exacerbate experimental chronic kidney disease via inflammatory and oxidative pathways involving NF-κB, ERK/p38 MAPK, and sirtuin-1
Researchers examined the effects of polystyrene microplastics on mice with chronic kidney disease and found that microplastic exposure worsened kidney dysfunction, inflammation, and tissue scarring. Even in healthy mice, microplastics reduced kidney filtration and increased markers of kidney damage. The study suggests that microplastic exposure may aggravate existing kidney conditions through inflammatory and oxidative stress pathways.
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.
From exposure to oncogenesis: a review on the multifaceted roles of microplastics in tumor initiation and progression
This review examined the evidence linking microplastic exposure to tumor initiation and progression, covering physical, chemical, and inflammatory mechanisms by which MPs may promote oncogenesis. The authors conclude that while current evidence is largely preclinical, accumulating data warrant serious concern about microplastics as environmental carcinogens.
Cytotoxicity and pro-inflammatory effect of polystyrene nano-plastic and micro-plastic on RAW264.7 cells.
Researchers found that polystyrene nano-plastics (80 nm) induced apoptosis and pro-inflammatory cytokine release in mouse macrophage RAW264.7 cells at lower concentrations than micro-plastics (3 μm), with nano-plastics also enhancing phagocytic activity and activating NF-kB signaling pathways more potently than their larger counterparts.
Polystyrene Microplastics Induce Radiotherapy Resistance in Lung Cancer by Suppressing Ferroptosis Through NF-κB Activation
Researchers found that polystyrene microplastics impaired radiotherapy efficacy in lung cancer cells by suppressing ferroptosis—a form of iron-dependent cell death—through NF-κB activation, providing the first evidence that microplastics may contribute to cancer therapy resistance.
Chronic Exposure to Polystyrene Nanoplastics Promotes Lung Cancer Progression via Activating Gluconeogenesis and Inhibiting Glycolysis
Researchers found that long-term exposure to polystyrene nanoplastics promoted lung cancer cell growth and migration by reprogramming cellular metabolism. The study suggests nanoplastics activate a specific metabolic pathway through the stress-response protein ATF3, shifting energy production in ways that enhance cancer cell proliferation.
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 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.
Supplemental exposure to polystyrene nanoplastics synergistically amplifies calcium oxalate crystal–induced injury to renal tubular epithelium, accelerating the formation of calcium oxalate kidney stones
Researchers found that polystyrene nanoplastics can synergistically worsen kidney stone formation when combined with calcium oxalate crystals, the primary component of kidney stones. The study detected microplastic components in human kidney stone samples and showed in both cell and animal models that nanoplastics amplify renal cell injury through ferroptosis and increased crystal adhesion.
Microplastics and Nanoplastics in Cancer Progression: Biology and Public Health
This review examines emerging evidence that microplastics and nanoplastics may contribute to cancer-related processes by crossing biological barriers and accumulating in tissues. The study highlights that these particles can cause oxidative stress, inflammation, DNA damage, and barrier dysfunction at the cellular level, and may promote tumor-supporting processes including angiogenesis and immune evasion.
Microscopic menace: exploring the link between microplastics and cancer pathogenesis
This review examines the growing evidence linking microplastic exposure to cancer development in humans. Microplastics can accumulate in the body and trigger inflammation, oxidative stress, and other biological changes associated with tumor growth. While more clinical research is needed, the review highlights that microplastics should be taken seriously as a potential factor in cancer risk.
Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice
This mouse study found that inhaling polystyrene microplastics caused serious lung damage, including inflammation, cell death, and scar tissue buildup. Smaller microplastics (1-5 micrometers) caused more harm than larger ones, and the damage worsened with longer exposure. The study identified a specific immune pathway (TLR2/NF-kB) through which inhaled microplastics trigger lung injury, raising concerns about the respiratory effects of airborne microplastics on humans.
Role of microplastics in the tumor microenvironment (Review)
This review examines how microplastics may help tumors grow by influencing the environment around cancer cells. Microplastics can interact with immune cells, connective tissue cells, blood vessel cells, and the tissue scaffolding around tumors in ways that may promote cancer progression and inflammation. While more research is needed, the findings raise important questions about whether chronic microplastic exposure could affect cancer development in humans.
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.