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Researchers found that microplastic exposure induced kidney injury resembling Heymann nephritis in rat models and worsened gut microbial imbalance. The study identified TFF3 as a novel upstream regulator associated with increased interleukin-17A levels following microplastic exposure. These findings suggest a potential link between microplastic exposure, gut dysbiosis, and kidney inflammation in animal models.
1. Microplastic exposure induced Heymann nephritis-like glomerular injury in rat models.2. Microplastic exposure exacerbated gut dysbiosis in Heymann nephritis rat models.3. The upstream regulator TFF3 as a novel mediator was associated with the upregulation of interleukin-17A following microplastic exposure.
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Raw data
AI summary Read the abstract
Researchers found that microplastic exposure induced kidney injury resembling Heymann nephritis in rat models and worsened gut microbial imbalance. The study identified TFF3 as a novel upstream regulator associated with increased interleukin-17A levels following microplastic exposure. These findings suggest a potential link between microplastic exposure, gut dysbiosis, and kidney inflammation in animal models.
Toxicological effects of microplastics in renal ischemia–reperfusion injury
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Researchers studied how microplastic exposure affects kidney injury and recovery in a mouse model of reduced blood flow to the kidneys. They found that microplastics worsened kidney damage by triggering inflammatory responses and disrupting cellular repair processes. The study suggests that microplastic accumulation in the body may increase vulnerability to kidney complications.
From exposure to injury: signaling mechanisms of microplastic-induced renal toxicity: an extensive review
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Researchers reviewed experimental and mechanistic evidence on how micro- and nanoplastics damage kidneys, synthesizing a framework in which oxidative stress, inflammasome activation, mitochondrial dysfunction, and profibrotic remodeling collectively drive nephron injury — while noting that standardized biomonitoring protocols and nanoscale detection methods remain critical unresolved challenges.
Single-cell RNA-seq analysis decodes the kidney microenvironment induced by polystyrene microplastics in mice receiving a high-fat diet
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Using advanced single-cell gene analysis, researchers found that mice fed both polystyrene microplastics and a high-fat diet suffered significantly worse kidney damage than either exposure alone. The combination reshaped the kidney's cellular environment, promoting scarring, triggering cancer-related pathways, and altering immune cell populations. This is particularly relevant to human health because many people are simultaneously exposed to microplastics through food and drink while also consuming high-fat diets.
Exploring the Mechanism of Kidney Injury in Mice Induced by High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Through the Kidney-Gut Axis
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In a mouse study, the combination of a high-fat diet and polystyrene nanoplastics caused worse kidney damage than either exposure alone, working through the kidney-gut connection. The nanoplastics plus high-fat diet disrupted gut bacteria, increased inflammation, and triggered a harmful immune response that traveled from the gut to the kidneys. This suggests that people who eat high-fat diets may be more vulnerable to kidney damage from nanoplastic exposure.
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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.