ArticleEndocrinology2012
Rapid estrogen receptor-mediated mechanisms determine the sexually dimorphic sensitivity of ventricular myocytes to 17β-estradiol and the environmental endocrine disruptor bisphenol A.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
56 citing papers in PubMed, 102 citations in OpenAlex.
- Exposure to bisphenols and phthalates and arterial stiffness in women of reproductive age: a New York City cohort analysis.Environment international · 2026Article
- Endocrine-disrupting chemicals exposure: cardiometabolic health risk in humans.Cardiovascular diabetology · 2025Review
- Developmental neurotoxicity of bisphenol F and bisphenol S in animal model systems: A literature review.Neurotoxicology · 2025Review
- Comparative cardiotoxicity assessment of bisphenol chemicals and estradiol using human induced pluripotent stem cell-derived cardiomyocytes.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Choice of experimental model determines translational impact: The link between bisphenol A and cardiotoxicity.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2023Article
- Current Evidence on Bisphenol A Exposure and the Molecular Mechanism Involved in Related Pathological Conditions.Pharmaceutics · 2023Review
- Acute exposure to low-dose bisphenol A delays cardiac repolarization in female canine heart - Implication for proarrhythmic toxicity in large animals.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2023Article
- Maternal perinatal exposure to bisphenol S induces an estrogenic like effect in glucose homeostasis in male offspring.Environmental toxicology · 2022Article
- Natural Products in Mitigation of Bisphenol A Toxicity: Future Therapeutic Use.Molecules (Basel, Switzerland) · 2022Review
- Endocrine-Disrupting Effects of Bisphenol A on the Cardiovascular System: A Review.Journal of xenobiotics · 2022Review
- Low doses of BPF-induced hypertrophy in cardiomyocytes derived from human embryonic stem cells via disrupting the mitochondrial fission upon the interaction between ERβ and calcineurin A-DRP1 signaling pathway.Cell biology and toxicology · 2022Article
- Characteristics of Bisphenol Cardiotoxicity: Impaired Excitability, Contractility, and Relaxation.Cardiovascular toxicology · 2022Review
- Potential Effects of Bisphenol A on the Heart and Coronary Artery of Adult Male Rats and the Possible Role of L-Carnitine.Journal of toxicology · 2022Article
- Endocrine disrupting chemicals interfere with decidualization of human primary endometrial stromal cellsFrontiers in endocrinology · 2022Article
- Key Characteristics of Cardiovascular Toxicants.Environmental health perspectives · 2021Article
- Changes Caused by Low Doses of Bisphenol A (BPA) in the Neuro-Chemistry of Nerves Located in the Porcine Heart.Animals : an open access journal from MDPI · 2021Article
- Update on the Health Effects of Bisphenol A: Overwhelming Evidence of Harm.Endocrinology · 2021Review
- Integrated Pharmacogenetics Analysis of the Three Fangjis Decoctions for Treating Arrhythmias Based on Molecular Network Patterns.Frontiers in cardiovascular medicine · 2021Article
- Data integration, analysis, and interpretation of eight academic CLARITY-BPA studies.Reproductive toxicology (Elmsford, N.Y.) · 2020Article
- A Simple Toxicokinetic Model Exhibiting Complex Dynamics and Nonlinear Exposure Response.Risk analysis : an official publication of the Society for Risk Analysis · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Previously we showed that 17β-estradiol (E(2)) and/or the xenoestrogen bisphenol A (BPA) alter ventricular myocyte Ca(2+) handing, resulting in increased cardiac arrhythmias in a female-specific manner. In the present study, the roles of estrogen receptors (ER) in mediating the rapid contractile and arrhythmogenic effects of estrogens were examined. Contractility was used as an index to assess the impact of E(2) or BPA on Ca(2+) handling in rodent ventricular myocytes. The concentration-response curve for the stimulatory effects of BPA and E(2) on female myocyte was inverted-U shaped. Detectable effects for each compound were observed at 10(-12) M, and the most efficacious concentrations for each were at 10(-9) M. Sensitivity to E(2) and BPA was not observed in male myocytes and was abolished in myocytes from ovariectomized females. Analysis using protein-conjugated E(2) suggests that these rapid actions are induced by membrane-associated receptors. Analysis using selective ER agonists and antagonists and a genetic ERβ knockout mouse model showed that ERα and ERβ have opposing actions in myocytes and that the balance between ERβ and ERα signaling is the prime regulator of the sex-specific sensitivity toward estrogens. The response of female myocytes to E(2) and BPA is dominated by the stimulatory ERβ-mediated signaling, and the absence of BPA and E(2) responsiveness in males is due to a counterbalancing-suppressive action of ERα. We conclude that the sex-specific sensitivity of myocytes to estrogens and the rapid arrhythmogenic effects of BPA and estradiol in the female heart are regulated by the balance between ERα and ERβ signaling.
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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.