ArticleBioMed research international2019
SLC9A3 Affects Vas Deferens Development and Associates with Taiwanese Congenital Bilateral Absence of the Vas Deferens.
Article in BioMed research international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Novel Candidate Genes Identified in Men with Congenital Absence of Vas Deferens without CFTR Gene Abnormalities.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- [Detection of pathogenic gene mutations in thirteen cases of congenital bilateral absence of vas deferens infertility patients].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2024Article
- NaInternational journal of molecular sciences · 2023Review
- Congenital Bilateral Absence of the Vas Deferens.Frontiers in genetics · 2022Review
- B6 Mouse Strain: The Best Fit for LPS-Induced Interstitial Cystitis Model.International journal of molecular sciences · 2021Article
- Genetics of Azoospermia.International journal of molecular sciences · 2021Review
- Genetics of the congenital absence of the vas deferens.Human genetics · 2021Review
- Article
- A novel hemizygous loss-of-function mutation in ADGRG2 causes male infertility with congenital bilateral absence of the vas deferens.Journal of assisted reproduction and genetics · 2020Article
- Genetics of Male Infertility - Present and Future: A Narrative Review.Journal of human reproductive sciencesReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe pathophysiology of Taiwanese congenital bilateral absence of the vas deferens (CBAVD) is different from that in Caucasians. In particular, major cystic fibrosis transmembrane conductance regulator (CFTR) mutations and cystic fibrosis are absent in the former. Instead, deficiency in solute carrier family 9 sodium/hydrogen exchanger isoform 3 (SLC9A3) may play a role by generating obstructive azoospermia and degraded epithelial structure in the reproductive tract.
objectivesThe objective of the study was to test whether SLC9A3 variants cause Taiwanese CBAVD. MATERIALS AND
methodsSix-month-old
resultsSLC9A3 was expressed and localized in the apical border of the epithelium of human vas deferens and glandular epithelium of the seminal vesicle. SLC9A3 deficiency specifically induces atrophy of vas deferens and unfolding of seminal vesicle mucosa in mice. Loss of SLC9A3 increased the incidence of CBAVD in humans from 3.1% to 37.9% (p < 0.001). Up to 75.9% of CBAVD patients carry at least one variant in either SLC9A3 or CFTR. DISCUSSION: Our findings build upon previous data associated with CBAVD pathogenesis. Here, we now report for the first time an association between CBAVD and loss of
conclusionThe data implicate loss of SLC9A3 as a basis of Taiwanese CBAVD and highlight SLC9A3 function in reproduction.
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