We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Issue Information‐ToC
AI summary Read the abstract
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 aggravates lipopolysaccharide-induced apoptosis in mouse kidney cells
More Papers Like This
Polystyrene nanoplastics aggravates lipopolysaccharide‐induced apoptosis in mouse kidney cells by regulating IRE1/XBP1 endoplasmic reticulum stress pathway via oxidative stress
AI summary Read the abstract
Researchers investigated whether polystyrene nanoplastics could worsen kidney cell damage caused by bacterial toxins in mice. They found that nanoplastics aggravated cell death by triggering oxidative stress, which activated a specific endoplasmic reticulum stress pathway involving the IRE1/XBP1 signaling cascade. The study suggests that combined exposure to nanoplastics and bacterial compounds may pose greater risks to kidney health than either stressor alone.
Polystyrene nanoplastics exacerbate gentamicin-induced nephrotoxicity in adult rat by activating oxidative stress, inflammation and apoptosis pathways
AI summary Read the abstract
Researchers co-exposed rats to polystyrene nanoplastics and the antibiotic gentamicin and found that the combination caused significantly greater kidney damage than either substance alone, amplifying oxidative stress, inflammation, and mitochondrial apoptosis in a synergistic manner.
Polystyrene nanoplastics induce apoptosis of human kidney proximal tubular epithelial cells via oxidative stress and MAPK signaling pathways
AI summary Read the abstract
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.
Nanoplastic toxicity and uptake in kidney cells: differential effects of concentration, particle size, and polymer type
AI summary Read the abstract
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 Microplastics Induce Nephrotoxicity via Oxidative Stress, Inflammation, Autophagy, and Ferroptosis
AI summary Read the abstract
Researchers reviewed the mechanisms by which polystyrene microplastics damage kidney tissue, finding that they converge on oxidative stress, NF-κB/NLRP3 inflammatory activation, and disruption of autophagy and ferroptosis pathways, with hub genes TP53 and TNF central to the toxic network and particle aging amplifying toxicity.
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.