ArticleReproductive toxicology (Elmsford, N.Y.)2025
Perfluoroalkyl substances (PFAS) exposure and preeclampsia risk: Impaired angiogenesis through suppression of VEGF signaling.
Article in Reproductive toxicology (Elmsford, N.Y.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The Placenta as a Target Organ for Poly- and Perfluoroalkyl Substances (PFASs): Molecular Mechanisms of Toxicity.International journal of molecular sciences · 2026Review
- Mitochondrial-targeted MitoQ attenuates PFOS-induced vasoconstriction and cAMP suppression in human placental arteries†.Biology of reproduction · 2026Article
- PFAS exposure and reproductive dysfunction: implications for outcomes in assisted reproductive technologies.Frontiers in endocrinology · 2026Review
- Prognostic value of uterine artery Doppler ultrasonography combined with serum PECAM-1 and PLGF levels and gut microbiota colony count for predicting outcomes in hypertensive disorder complicating pregnancy patients.Frontiers in medicine · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
Per- and polyfluoroalkyl substances (PFAS) are linked to preeclampsia (PE), a condition involving abnormal angiogenesis. Prior research on this association has been inconclusive. We investigated the relationship between maternal PFAS exposure and PE risk in Wisconsin. We also examined if PFAS disrupts angiogenesis and, if so, what mechanisms are involved. We conducted a case-control study with 40 PE cases and 40 controls. Maternal serum was analyzed for 38 different PFAS compounds using LC MS/MS. Functional in vitro experiments assessed PFOS effects on angiogenesis and mechanisms. Maternal serum samples from women with PE exhibited significantly higher PFOS and PFHPS concentrations than controls. After adjusting for confounders, each log-scale IQR increase in PFOS and PFHPS concentrations was associated with a 7.18-fold (95 % CI: 2.24, 23.0) and 5.40-fold (95 % CI: 1.81, 16.1) higher odds of PE, respectively. Furthermore, PFOS and PFHPS were positively associated with sFLT1 levels and the sFLT1/PLGF ratio. In vitro experiments revealed that PFOS exposure impaired HUVEC proliferation, migration, and tube formation, essential processes for angiogenesis. The membrane-based antibody array showed that PFOS decreased expression of multiple angiogenic proteins, including I-TAC, uPAR, VEGFR2, MMP-1, IL-1α, Angiopoietin-2, IL-1β, PECAM-1, TIE-2, and TIMP-2. The qPCR analysis demonstrated that PFOS decreased VEGFR2, the upstream target of VEGF, at the transcriptional level. In conclusion, elevated PFAS, especially PFOS and PFHPS, are linked to increased PE risk. PFOS may suppress angiogenesis via attenuated VEGFR2-mediated signaling, providing a molecular mechanism linking PFAS and PE pathogenesis.
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