ArticleThe Journal of clinical investigation2018
Constitutively active follicle-stimulating hormone receptor enables androgen-independent spermatogenesis.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- Does hormonal therapy improve sperm retrieval rates in men with non-obstructive azoospermia: a systematic review and meta-analysis.Human reproduction update · 2022Pooled it
- Review
- Article
- Single-chain human Follicle-stimulating hormone promotes ovarian and testicular growth and improves pregnancy performance in mice.PloS one · 2026Article
- Monoclonal antibody potentiating gonadotropin activity in vitro and in vivo in male and female rats and in ewes.Reproduction (Cambridge, England) · 2025Article
- Pharmacogenomic of LH and its receptor: are we ready for clinical practice?Reproductive biology and endocrinology : RB&E · 2025Review
- Improvement of Late-Onset Hypogonadism Symptoms of FermentedNutrients · 2024Article
- Hormone Regulation in Testicular Development and Function.International journal of molecular sciences · 2024Review
- Revisiting the gonadotropic regulation of mammalian spermatogenesis: evolving lessons during the past decade.Frontiers in endocrinology · 2023Review
- Impact of add-back FSH on human and mouse prostate following gonadotropin ablation by GnRH antagonist treatment.Endocrine connections · 2022Article
- Gonadotropins treatment prior to microdissection testicular sperm extraction in non-obstructive azoospermia: a single-center cohort study.Reproductive biology and endocrinology : RB&E · 2022Article
- Single-cell RNA sequencing of adult rat testes after Leydig cell elimination and restoration.Scientific data · 2022Article
- Reversible hypogonadotropic hypogonadism in men with the fertile eunuch/Pasqualini syndrome: A single-center natural history study.Frontiers in endocrinology · 2022Article
- The Roles of Luteinizing Hormone, Follicle-Stimulating Hormone and Testosterone in Spermatogenesis and Folliculogenesis Revisited.International journal of molecular sciences · 2021Review
- Article
- The Luteinizing Hormone Receptor Knockout Mouse as a Tool to Probe the In Vivo Actions of Gonadotropic Hormones/Receptors in Females.Endocrinology · 2021Article
- Hormonal Treatment of Men with Nonobstructive Azoospermia: What Does the Evidence Suggest?Journal of clinical medicine · 2021Review
- Androgen Actions in the Testis and the Regulation of Spermatogenesis.Advances in experimental medicine and biology · 2021Review
- Article
- Recent advances in understanding gonadotropin signaling.Faculty reviews · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 7 institutions in 4 countries.
Funding
Abstract
Spermatogenesis is regulated by the 2 pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This process is considered impossible without the absolute requirement of LH-stimulated testicular testosterone (T) production. The role of FSH remains unclear because men and mice with inactivating FSH receptor (FSHR) mutations are fertile. We revisited the role of FSH in spermatogenesis using transgenic mice expressing a constitutively strongly active FSHR mutant in a LH receptor-null (LHR-null) background. The mutant FSHR reversed the azoospermia and partially restored fertility of Lhr-/- mice. The finding was initially ascribed to the residual Leydig cell T production. However, when T action was completely blocked with the potent antiandrogen flutamide, spermatogenesis persisted. Hence, completely T-independent spermatogenesis is possible through strong FSHR activation, and the dogma of T being a sine qua non for spermatogenesis may need modification. The mechanism for the finding appeared to be that FSHR activation maintained the expression of Sertoli cell genes considered androgen dependent. The translational message of our findings is the possibility of developing a new strategy of high-dose FSH treatment for spermatogenic failure. Our findings also provide an explanation of molecular pathogenesis for Pasqualini syndrome (fertile eunuchs; LH/T deficiency with persistent spermatogenesis) and explain how the hormonal regulation of spermatogenesis has shifted from FSH to T dominance during evolution.
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.