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Polystyrene microplastics facilitate renal fibrosis through accelerating tubular epithelial cell senescence
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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.
Microplastics (MPs), emerging contaminants, are easily transported and enriched in the kidney, suggesting the kidney is susceptible to the toxicity of MPs. In this study, we explored the toxicity of MPs, including unmodified polystyrene (PS), negative-charged PS-SOH, and positive-charged PS-NH MPs, in mice models for 28 days at a human equivalent concentration. The results showed MPs significantly increased levels of UREA, urea nitrogen (BUN), creatinine (CREA), and uric acid (UA) levels in serum and white blood cells, protein, and microalbumin in urine. In the kidney, MPs triggered persistent inflammation and renal fibrosis, which was caused by the increased senescence of tubular epithelial cells. Moreover, we identified the critical role of the Klotho/Wnt/β-catenin signaling pathway in the process of MPs induced senescence of tubular epithelial cells, promoting the epithelial-mesenchymal transformation of epithelial cells. MPs supported the secretion of TGF-β1 by senescent epithelial cells and induced the activation of renal fibroblasts. On the contrary, restoring the function of Klotho can alleviate the senescence of epithelial cells and reverse the activation of fibroblasts. Thus, our study revealed new evidence between MPs and renal fibrosis, and adds an important piece to the whole picture of the plastic pollution on people's health.
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Chronic exposure to polystyrene microplastics induces renal fibrosis via ferroptosis
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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.
Polystyrene Microplastics Activate Noncanonical TGF-β Signaling and Metabolomic Reprogramming to Promote Epithelial-Mesenchymal Transition and Fibrosis in the Kidney
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In a mouse study, tiny plastic particles called microplastics (commonly found in food, water, and even human organs) built up in the kidneys and triggered changes linked to scarring and declining kidney function, along with shifts in metabolism similar to those seen in chronic kidney disease. While this research was done in mice and cells rather than people, it adds to growing evidence that the microplastics we're constantly exposed to may pose real risks to kidney health over time.
Polystyrene microplastic-induced extracellular vesicles cause kidney-related effects in the crosstalk between tubular cells and fibroblasts
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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 Chronic Exposure Aggravates Diabetic Kidney Injury in mice: role of mtROS/Sirt1 axis mediated renal tubular senescence
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In a study on diabetic mice, tiny plastic particles called nanoplastics (similar to those found in everyday plastic pollution) built up in the kidneys and made diabetes-related kidney damage worse by stressing out the cells' energy-producing mitochondria, causing kidney cells to age faster than normal. This matters because diabetic nephropathy already affects millions of people, and this research suggests that everyday exposure to plastic particles could be a hidden factor that speeds up kidney damage in an already vulnerable population, though more research is needed to confirm this happens in humans too.
Polystyrene Microplastics Activate Noncanonical TGF-β Signaling and Metabolomic Reprogramming to Promote Epithelial-Mesenchymal Transition and Fibrosis in the Kidney
AI summary Read the abstract
Scientists fed mice tiny plastic particles (the kind found in everyday products, and already detected in human kidneys) and found they built up in the kidneys, damaged kidney tissue, and triggered changes linked to scarring and reduced kidney function. The plastics also threw off the body's metabolism in ways that mirror patterns seen in chronic kidney disease. While this study was done in mice and cells rather than humans, it adds to growing evidence that microplastic exposure may pose real risks to kidney health over time.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.