ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Ablation of the canonical testosterone production pathway via knockout of the steroidogenic enzyme HSD17B3, reveals a novel mechanism of testicular testosterone production.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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
33 citing papers in PubMed, 48 citations in OpenAlex.
- Post-translational modification of proteins in the human testis development pathway.Human reproduction update · 2026Review
- Decoding cytarabine-induced damage in the prepubertal testis: A multi-omics atlas of ecosystem and inheritance.iScience · 2026Article
- Effects of dendrobium nobile polysaccharide on reproductive performance, hormone levels, antioxidant capacity, and testicular metabolism of aged roosters.Poultry science · 2026Article
- Clinical management and genetic variation analysis of patients with 17β-hydroxysteroid dehydrogenase deficiency.The Journal of international medical research · 2026Article
- Female Mice with HSD17B1 Inactivation Show Mild Hyperandrogenism without Notable Impact on Reproductive Function or Bone.Endocrinology · 2025Article
- Functional Analysis of HSD17B3-Deficient Male Mice Reveals Roles for HSD17B7 and HSD17B12 in Testosterone Biosynthesis.Endocrinology · 2025Article
- Prenatal bisphenol A exposure causes sperm quality and functional defects via Leydig cell impairment and meiosis arrest in mice offspring.Scientific reports · 2025Article
- Therapeutic Potential ofInternational journal of endocrinology · 2025Article
- Ameliorative effect of Melatonin on 5-Fluorouracil-induced reproductive toxicity in male rats.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2024Article
- Compensatory mechanisms that maintain androgen production in mice lacking key androgen biosynthetic enzymes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Crafting Contours: A Comprehensive Guide to Scrotal Reconstruction.Life (Basel, Switzerland) · 2024Review
- The mitochondrial protease PARL is required for spermatogenesis.Communications biology · 2024Article
- Dynamics of HSD17B3 expression in human fetal testis: implications for the role of Sertoli cells in fetal testosterone biosynthesis.Frontiers in cell and developmental biology · 2024Article
- Loss of NR5A1 in mouse Sertoli cells after sex determination changes cellular identity and induces cell death by anoikis.Development (Cambridge, England) · 2023Article
- Epigenetic determinants of reproductive potential augment the predictive ability of the semen analysis.F&S science · 2023Article
- Male reproductive traits are differentially affected by dietary macronutrient balance but unrelated to adiposity.Nature communications · 2023Article
- 4-Methylumbelliferone Targets Revealed by Public Data Analysis and Liver Transcriptome Sequencing.International journal of molecular sciences · 2023Article
- Article
- New Insights into Testosterone Biosynthesis: Novel Observations from HSD17B3 Deficient Mice.International journal of molecular sciences · 2022Review
- A Novel Model Using AAV9-Cre to Knockout Adult Leydig Cell Gene Expression Reveals a Physiological Role of Glucocorticoid Receptor Signalling in Leydig Cell Function.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
Abstract
Male development, fertility, and lifelong health are all androgen-dependent. Approximately 95% of circulating testosterone is synthesized by the testis and the final step in this canonical pathway is controlled by the activity of the hydroxysteroid-dehydrogenase-17-beta-3 (HSD17B3). To determine the role of HSD17B3 in testosterone production and androgenization during male development and function we have characterized a mouse model lacking HSD17B3. The data reveal that developmental masculinization and fertility are normal in mutant males. Ablation of HSD17B3 inhibits hyperstimulation of testosterone production by hCG, although basal testosterone levels are maintained despite the absence of HSD17B3. Reintroduction of HSD17B3 via gene-delivery to Sertoli cells in adulthood partially rescues the adult phenotype, showing that, as in development, different cell-types in the testis are able to work together to produce testosterone. Together, these data show that HS17B3 acts as a rate-limiting-step for the maximum level of testosterone production by the testis but does not control basal testosterone production. Measurement of other enzymes able to convert androstenedione to testosterone identifies HSD17B12 as a candidate enzyme capable of driving basal testosterone production in the testis. Together, these findings expand our understanding of testosterone production in males.
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.