ArticleCommunications biology2024
Bisphenol S causes excessive estrogen synthesis by activating FSHR and the downstream cAMP/PKA signaling pathway.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- FSHR and LHR functional compensation reveals the mechanism and treatment of Ovarian Hyperstimulation Syndrome.Nature communications · 2026Article
- Placental Steroid Hormones in Preeclampsia: Multilayered Regulation of Endocrine Pathogenesis.Endocrine reviews · 2026Review
- Bisphenol A Alternatives in Follicular Fluid: Novel Risk Factors for Ovarian Reserve Dysfunction.ACS omega · 2026Article
- Migration of Bisphenol A and Its Derivatives From Epoxy Coatings and Demand for BPA-NI Products: Scientific Insights and Perspectives Leading to Regulation (EU) 2024/3190.Chemistry, an Asian journal · 2025Review
- EGF receptor in organ development, tissue homeostasis and regeneration.Journal of biomedical science · 2025Review
- The effects of bisphenol A and its analogs on steroidogenesis in MA-10 Leydig cells and KGN granulosa cells†.Biology of reproduction · 2025Article
- Reduced bioenergetics and mitochondrial fragmentation in human primary cytotrophoblasts induced by an EGFR-targeting chemical mixture.Chemosphere · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Estrogen excess in females has been linked to a diverse array of chronic and acute diseases. Emerging research shows that exposure to estrogen-like compounds such as bisphenol S leads to increases in 17β-estradiol levels, but the mechanism of action is unclear. The aim of this study was to reveal the underlying signaling pathway-mediated mechanisms, target site and target molecule of action of bisphenol S causing excessive estrogen synthesis. Human ovarian granulosa cells SVOG were exposed to bisphenol S at environmentally relevant concentrations (1 μg/L, 10 μg/L, and 100 μg/L) for 48 h. The results confirms that bisphenol S accumulates mainly on the cell membrane, binds to follicle stimulating hormone receptor (FSHR) located on the cell membrane, and subsequently activates the downstream cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) signaling pathway, leading to enhanced conversion of testosterone to 17β-estradiol. This study deepens our knowledge of the mechanisms of environmental factors in pathogenesis of hyperestrogenism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.