ArticleNature communications2026
Genetic variations interact with polybrominated diphenyl ether exposure to alter lipid homeostasis.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
25 authors.
Funding
Abstract
Polybrominated diphenyl ethers (PBDEs) are implicated in dyslipidemia, but the molecular basis of individual susceptibility remains elusive. Here we report an analysis based on the China National Human Biomonitoring cohort, where we integrate exposome, genomic, and metabolomic data to identify 3,571 genetic variants that interact with PBDE exposure to influence dyslipidemia risk. Metabolomic analysis highlights glycine and glycerophosphate as key mediators. A polygenic risk score derived from these PBDE-interactive variants significantly enhances dyslipidemia prediction in highly exposed individuals. Among these, rs9869609 emerges as a candidate causal variant, showing the strongest association with hypercholesterolemia risk (β = 1.18, FDR = 0.0078). Further functional validation using single-base CRISPR/Cas9 editing reveals that the rs9869609-G allele downregulates SLC6A20 expression by strengthening BHLHE40 binding, which further impairs glycine transport and promotes cholesterol accumulation, particularly under 2,2',4,4'-Tetrabromodiphenyl ether exposure. Collectively, our study elucidates a gene-environment interaction mechanism through which genetic variants modulate lipid metabolism in response to PBDE exposure.
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