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Unveiling the molecular toxicity of plasticizers derived from microplastics (DMP and DEP) in diabetic kidney disease: integrative insights from network toxicology and multi-omics analysis
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Scientists found that two chemicals commonly released from microplastics (used to make plastics flexible) can damage kidney cells in lab tests, and this damage got worse when combined with high blood sugar levels similar to those seen in diabetes. This early-stage research points to specific genes that may explain how these plastic chemicals harm kidney health, but the findings come from cell studies, not humans, so more research is needed before we know if this applies to real-world diabetic kidney disease. Still, it raises important questions about whether everyday plastic exposure could compound health risks for people with diabetes.
Background Diabetic kidney disease (DKD) is a prevalent microvascular complication with limited therapeutic options. This study aimed to identify biomarkers associated with microplastic-associated plasticizers in DKD and to explore their potential molecular mechanisms. Methods Publicly available datasets were integrated for biomarker discovery, followed by experimental validation in human proximal tubular epithelial cells (HK-2). Pathway enrichment and immune infiltration analyses were performed to characterize the biological relevance of the identified biomarkers. Molecular docking and molecular dynamics simulations were used to evaluate the predicted interactions between the biomarkers and the plasticizers dimethyl phthalate (DMP) and diethyl phthalate (DEP). Single-cell transcriptomic analysis was further conducted to characterize the cell-type-specific expression of the identified biomarkers. Results CASP3, PTGES, and SLC6A2 were identified as candidate biomarkers. Pathway analysis revealed that these genes were notably enriched in oxidative phosphorylation, while immune infiltration analysis indicated a strong correlation between PTGES and memory B cells. Molecular docking and molecular dynamics simulations predicted stable interactions between the biomarkers and DMP and DEP. In vitro experiments further showed that DMP and DEP exposure reduced HK-2 cell viability, promoted apoptosis, and dysregulated the expression of CASP3, PTGES, and SLC6A2. Notably, these toxic effects were exacerbated under high-glucose conditions, suggesting an enhanced combined effect between the diabetic milieu and plasticizer-induced stress. Single-cell transcriptomic analysis further indicated predominant CASP3 expression in proximal convoluted tubule (PCT) cells. Conclusions This study provides a hypothesis-generating framework by identifying CASP3, PTGES, and SLC6A2 as potential DKD biomarkers that are computationally predicted and experimentally shown to be regulated by microplastic-associated plasticizers. These findings suggest potential molecular links between plasticizer exposure and DKD-related cellular injury; however, their exposure-dependent relevance and mechanistic roles in human DKD require further validation.
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This computational study used bioinformatics to explore how polyethylene terephthalate (PET) microplastics might worsen diabetic kidney disease. The analysis identified key genes and inflammatory pathways that are affected by both PET microplastics and kidney damage in diabetes. The findings suggest that microplastic exposure could accelerate kidney problems in people who already have diabetes, though lab and clinical studies are needed to confirm this.
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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.
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Tiny plastic particles have been found in human blood, urine, and even kidney tissue, and lab studies show they can stress kidney cells and potentially contribute to inflammation and scarring. This review pulls together what scientists currently know, but it's clear we still don't have solid proof that microplastics actually cause kidney disease in people, more research is needed, especially for those already dealing with kidney problems or dialysis, before we can say how worried to be.
Network Toxicology and Multi-omics Analysis
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This entry contains data and code supporting a study that used computational methods to investigate how microplastics may worsen diabetic kidney disease at the molecular level. The parent study suggests microplastics could affect kidney health through specific biological pathways, though this entry itself is a data repository rather than a full paper.
Microplastics and the Kidney: A Narrative Review of Human Evidence, Molecular Mechanisms of Cell Injury, and Future Directions
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This review summarizes existing research on how tiny plastic particles might affect kidney health. It describes how plastics entering cells can trigger stress and damage in lab studies, and notes that human studies have found microplastics in urine and kidney tissue, linked to early signs of kidney damage, though evidence remains limited.
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