We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene Microplastics Activate Noncanonical TGF-β Signaling and Metabolomic Reprogramming to Promote Epithelial-Mesenchymal Transition and Fibrosis in the Kidney
Original title: Polystyrene MicroplasticsActivate Noncanonical TGF‑βSignaling and Metabolomic Reprogramming to Promote Epithelial-MesenchymalTransition 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.
Polystyrene microplastics (PS-MPs) have been detected in human kidneys, raising concerns about their potential health risks. In this study, we investigated the effects of 1 μm PS-MPs in BALB/c mice and NRK-52E cells. After 28 days of exposure to PS-MPs (0.1, 1, and 10 mg/kg), we observed decreased body weight and elevated levels of serum creatinine and other kidney injury markers. PS-MPs accumulated in the kidney, as confirmed by MicroRaman spectroscopy, and caused significant histopathological changes and an increase in mesenchymal markers (α-SMA, fibronectin, collagen IV, and vimentin) while reducing the epithelial marker, E-Cadherin. Further mechanistic studies revealed the activation of the noncanonical TGFβ pathway involving P38MAPK, Akt, STAT3, STAT5, and NF-κB, which led to epithelial-mesenchymal transition (EMT) and the early onset of kidney fibrosis. Moreover, NMR-based metabolomics indicated changes in metabolites involved in energy and amino-acid metabolism, including decreased levels of branched-chain amino acids (BCAAs; leucine, isoleucine, and valine), phenylalanine, and increased glutamine levels. This altered metabolomic pathways, including the biosynthesis of phenylalanine, tyrosine, and tryptophan, as well as phenylalanine metabolism, which have been previously associated with chronic kidney disease. Overall, this study indicates that exposure to PS-MPs may jeopardize renal health by altering metabolic pathways and signaling related to EMT and kidney fibrosis.
More Papers Like This
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
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 microplastics facilitate renal fibrosis through accelerating tubular epithelial cell senescence
AI summary Read the abstract
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.
PS-MPs promotes the progression of inflammation and fibrosis in diabetic nephropathy through NLRP3/Caspase-1 and TGF-β1/Smad2/3 signaling pathways.
AI summary Read the abstract
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 microplastic-induced extracellular vesicles cause kidney-related effects in the crosstalk between tubular cells and fibroblasts
AI summary Read the abstract
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.
Micro- and nanoplastics and the kidney: exposure pathways, toxicokinetics, and pathophysiological insights
AI summary Read the abstract
Tiny plastic particles from our air, water, and food—called micro- and nanoplastics—can enter our bodies and travel to the kidneys, where studies show they may cause cell damage, inflammation, and scarring over time. This review pulls together existing research on how these plastics get into our system and harm kidney tissue, suggesting that everyday plastic exposure could be an overlooked risk factor for kidney disease. More research is needed, but this is an early signal that reducing plastic exposure might matter for long-term kidney health.
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.