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Long-term micro/nanoplastic ingestion promotes sepsis by worsening kidney damage: a transcriptomics and metabolomics study
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Researchers found that long-term ingestion of micro- and nanoplastics worsened kidney damage in septic mice and reduced survival rates, with multi-omics analysis identifying five genes — Srm, Pycr2, Arg2, Asns, and Psat1 — as likely key mediators linking plastic exposure to aggravated sepsis outcomes.
Our study finds that smaller-sized plastics affect the survival of septic mice by damaging and aggravating kidney injury. Multi-omics analysis has revealed that five genes—Srm, Pycr2, Arg2, Asns, and Psat1—may play key roles in this process.
More Papers Like This
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.
The microplastics exposure induce the kidney injury in mice revealed by RNA-seq
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In a mouse study, microplastics of different sizes caused kidney injury including inflammation, oxidative stress, and scarring (fibrosis) after long-term exposure. The smallest particles (80 nanometers) altered immune-related genes, while larger particles disrupted genes tied to the body's internal clock. This research provides evidence that microplastics accumulating in the body over time could contribute to kidney disease in mammals, including humans.
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.
Exploring the Mechanismof Kidney Injury in Mice Inducedby High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Throughthe Kidney-Gut Axis
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This mouse study found that combining a high-fat diet with polystyrene nanoplastic exposure (100 nm, 25 mg/kg/day) worsened kidney toxicity beyond high-fat diet alone, with the combination disrupting lipid metabolism via tryptophan and glycerophospholipid pathways and exacerbating gut microbiota dysbiosis through the kidney-gut axis.
Multi-omics and genetic prioritization identify candidate molecular links between micro- and nanoplastics-associated signatures and chronic kidney disease
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Scientists used advanced computer modeling and lab tests to explore how tiny plastic particles (microplastics) found in our bodies might contribute to chronic kidney disease. They identified specific genes and biological pathways linking plastic exposure to kidney damage, and confirmed in lab-grown kidney cells that polystyrene microplastics can trigger changes linked to kidney scarring. While this is early-stage research that doesn't prove plastics directly cause kidney disease in people, it offers promising leads for understanding—and potentially preventing—environmentally-driven kidney damage.
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.