Polystyrene microplastics disrupt kidney organoid development via oxidative stress and Bcl-2/Bax/caspase pathway.

Microplastics (MPs), particularly polystyrene microplastics (PS-MPs), have emerged as significant environmental pollutants with potential risks to human health. Their presence has been detected in human tissues, including blood and placental tissue, raising concerns about developmental effects. However, MPs' effects on the development of human organs are still mostly unknown.

Polystyrene microplastics induce nephrotoxicity through DDIT4-mediated autophagy and apoptosis.

Microplastics (MPs), plastic particles smaller than 5 mm, have garnered increasing attention due to their pervasive presence in the environment and potential health risks. While their accumulation in various organs, including the liver, kidneys, and intestines, is well-documented, the specific mechanisms they affect kidney development remain unclear. This study investigated the nephrotoxic effects of 1 μm polystyrene microplastics (PS-MPs) using a 3D kidney organoid model derived from human pluripotent stem cells, focusing on the molecular pathways involved.

Microplastics induce human kidney development retardation through ATP-mediated glucose metabolism rewiring.

Recent research has revealed an accumulation of microplastics (MPs) in the environment and human tissues, giving rise to concerns about their potential toxicity. The kidney is a vital organ responsible for various physiological functions. Early kidney development is crucial for ensuring proper structure and function.

Microplastics exposure disrupts nephrogenesis and induces renal toxicity in human iPSC-derived kidney organoids.

Microplastics (MPs) have emerged as a pervasive environmental pollutant of global concern. Their detection within the human placenta and fetal organs has prompted apprehension regarding the potential hazards of MPs during early organogenesis. The kidney, a vital multifunctional organ, is susceptible to damage from MPs in adulthood.