ArticleThe application of clinical genetics2025
The Impact of FSHR Polymorphisms (rs6165 and rs6166) on Ovarian Response to Stimulation in Infertile Women with Diminished Ovarian Reserve.
Article in The application of clinical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Molecular analysis of FSHR rs6166 polymorphism and oxidative stress parameters in women with polycystic ovary syndrome.Molecular biology reports · 2026Article
- Significance of Follicle-Stimulating Hormone Receptor Gene Single-Nucleotide Polymorphism rs6165/rs6166 Analysis for Infertility-Associated Ovarian Disease Susceptibility Prediction and Optimized Individualized Ovulation Induction/Ovarian Stimulation.Diagnostics (Basel, Switzerland) · 2026Review
- Assessment indicators of ovarian response during controlled ovarian stimulation: influencing factors and clinical value.Frontiers in endocrinology · 2026Review
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Authors and funding
8 authors.
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Abstract
Background: Diminished ovarian reserve (DOR) remains a significant challenge in IVF, as it is closely associated with poor ovarian response. Beyond well-established predictive of ovarian response, genetic polymorphisms in the FSH receptor (FSHR) gene rs6165 and rs6166 have been reported as potential markers. Purpose: Evaluating the expression of FSHR rs6165 and rs6166 in DOR patients and their impact on ovarian response to stimulation. Materials and Methods: This prospective cross-sectional included 79 DOR patients (AMH < 1.2 ng/mL and/or AFC < 5) undergoing IVF treatment at the National Hospital of Obstetrics and Gynecology, Vietnam. GnRH antagonist protocol was applied, using alpha follitropin with individualized dosages combined with clomiphene citrate, followed by dual-trigger ovulation induction. FSHR rs6165 and rs6166 were genotyped by Next-Generation Sequencing (NGS) assays, with Sanger sequencing for validation. Ovarian response was assessed based on follicular development and oocyte retrieval. Results: The overall prevalence of the rs6165 and rs6166 polymorphisms was 10.1% (8/79), with strong linkage disequilibrium observed between the two loci (OR = 490, p < 0.0001). No significant differences in age, AMH, baseline FSH, and AFC were found in all genotypes (AA, AG, GG) of rs6165 and rs6166. In the rs6165 dominant model, patients with G alleles (AG/GG) had lower total oocyte retrieval, FOI and FORT than the AA genotype. In rs6166 codominant, dominant, and recessive models, the GG phenotype retrieved fewer oocytes (p1 = 0.02, p2 = 0.03, p3 = 0.01). FORT was significantly lower in G allele carriers (AG/GG) than AA (p = 0.04). Conclusion: In the diminished ovarian reserve patients, FSHR rs6165 and rs6166 were associated with ovarian response to stimulation in IVF treatment. Specifically, the presence of G alleles in both rs6165 and rs6166 was correlated with reduced oocyte retrieval, independent of baseline ovarian reserve markers.
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