ReviewFrontiers in endocrinology2015
Nuclear receptors and endocrine disruptors in fetal and neonatal testes: a gapped landscape.
Review in Frontiers in endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Unraveling the Androgen Receptor's Role in Hypospadias: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2026Pooled it
- Review
- Exposure to Bisphenol B and S Increases the Risk of Male Reproductive Dysfunction in Middle Age.International journal of molecular sciences · 2025Article
- Disruption of PPARG Activity and CPT1A Regulation by Bisphenol A: Implications for Hepatic Lipid Metabolism.Journal of cellular and molecular medicine · 2025Article
- Estrogenic endocrine disruptor exposure directly impacts erectile function.Communications biology · 2024Article
- Maternal Exposure to Per- and Polyfluoroalkyl Substances (PFAS) and Male Reproductive Function in Young Adulthood: Combined Exposure to Seven PFAS.Environmental health perspectives · 2022Article
- Ovine fetal testis stage-specific sensitivity to environmental chemical mixtures.Reproduction (Cambridge, England) · 2022Article
- Impact ofFrontiers in toxicology · 2022Article
- Unexpected Interacting Effects of Physical (Radiation) and Chemical (Bisphenol A) Treatments on Male Reproductive Functions in Mice.International journal of molecular sciences · 2021Article
- Use of the Adverse Outcome Pathway (AOP) framework to evaluate species concordance and human relevance of Dibutyl phthalate (DBP)-induced male reproductive toxicity.Reproductive toxicology (Elmsford, N.Y.) · 2020Review
- Review
- All-trans Retinoic Acid Disrupts Development in Ex Vivo Cultured Fetal Rat Testes. II: Modulation of Mono-(2-ethylhexyl) Phthalate Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Crosstalk between BPA and FXRα Signaling Pathways Lead to Alterations of Undifferentiated Germ Cell Homeostasis and Male Fertility Disorders.Stem cell reports · 2018Article
- Effects of environmental Bisphenol A exposures on germ cell development and Leydig cell function in the human fetal testis.PloS one · 2018Article
- Risks and benefits related to alimentary exposure to xenoestrogens.Critical reviews in food science and nutrition · 2017Review
- Chlorinated biphenyls effect on estrogen-related receptor expression, steroid secretion, mitochondria ultrastructure but not on mitochondrial membrane potential in Leydig cells.Cell and tissue research · 2017Article
- Chronic low-dose exposure to a mixture of environmental endocrine disruptors induces microRNAs/isomiRs deregulation in mouse concomitant with intratesticular estradiol reduction.Scientific reports · 2017Article
- A Case-Control Study of Maternal Polybrominated Diphenyl Ether (PBDE) Exposure and Cryptorchidism in Canadian Populations.Environmental health perspectives · 2017Article
- Long-term exposure to a 'safe' dose of bisphenol A reduced protein acetylation in adult rat testes.Scientific reports · 2017Article
- Endocrine Aspects of Environmental "Obesogen" Pollutants.International journal of environmental research and public health · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the last decades, many studies reported that male reproductive disorders are increasing among humans. It is currently acknowledged that these abnormalities can result from fetal exposure to environmental chemicals that are progressively becoming more concentrated and widespread in our environment. Among the chemicals present in the environment (air, water, food, and many consumer products), several can act as endocrine disrupting compounds (EDCs), thus interfering with the endocrine system. Phthalates, bisphenol A (BPA), and diethylstilbestrol (DES) have been largely incriminated, particularly during the fetal and neonatal period, due to their estrogenic and/or anti-androgenic properties. Indeed, many epidemiological and experimental studies have highlighted their deleterious impact on fetal and neonatal testis development. As EDCs can affect many different genomic and non-genomic pathways, the mechanisms underlying the adverse effects of EDC exposure are difficult to elucidate. Using literature data and results from our laboratory, in the present review, we discuss the role of classical nuclear receptors (genomic pathway) in the fetal and neonatal testis response to EDC exposure, particularly to phthalates, BPA, and DES. Among the nuclear receptors, we focused on some of the most likely candidates, such as peroxisome-proliferator activated receptor (PPAR), androgen receptor (AR), estrogen receptors (ERα and β), liver X receptors (LXR), and small heterodimer partner (SHP). First, we describe the expression and potential functions (based on data from studies using receptor agonists and mouse knockout models) of these nuclear receptors in the developing testis. Then, for each EDC studied, we summarize the main evidences indicating that the reprotoxic effect of each EDC under study is mediated through a specific nuclear receptor(s). We also point-out the involvement of other receptors and nuclear receptor-independent pathways.
Indexed as
Identifiers
What OpenQuestion holds
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.