ArticleBMC endocrine disorders2026
AMH specifically targets neuronal AMHR2 to modulate the progression of polycystic ovary syndrome.
Article in BMC endocrine disorders, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Molecular mechanisms and multi-organ regulatory roles of anti-Müllerian hormone in female reproduction.Communications biology · 2026Review
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Abstract
backgroundPolycystic ovary syndrome (PCOS) is a prevalent reproductive endocrine disorder among women of childbearing age, characterized by elevated serum anti-Müllerian hormone (AMH) levels as a key biomarker. This study primarily investigates the tissue-specific expression of AMHR2 (the receptor for AMH) and its mechanistic role in PCOS pathogenesis.
methodsIn this study, we employed a two-phase experimental approach to investigate the tissue-specific roles of AMHR2 in PCOS pathogenesis. First, we established extra-ovarian (Ex-AMHR2) and intra-ovarian (In-AMHR2) AMHR2 expression models through reciprocal ovarian transplantation between wild-type (WT) and conventional AMHR2 knockout (AMHR2−/−) female mice. Second, we systematically compared tissue-specific effects using conditional knockout models targeting either neuronal (Neur-AMHR2−/−) or ovarian (Ovary-AMHR2−/−) AMHR2 expression. All experimental groups received standardized AMH intervention (0.12 mg/kg, i.p., twice weekly for 4 weeks). Comprehensive evaluations included: (1) reproductive cyclicity monitoring and ovarian index calculation; (2) ELISA quantification of serum AMH, LH, FSH, T, E1, and E2 levels with derived hormonal ratios; (3) histopathological assessment of ovarian morphology via H&E staining with follicular enumeration; and (4) molecular analyses of oocyte quality markers (GDF9, BMP15) at both protein (Western blot) and mRNA (qPCR) levels. This integrated experimental paradigm enabled multi-dimensional characterization of compartmentalized AMHR2 signaling in PCOS development.
resultsBy comparing mice with intraovarian and extraovarian expression of AMHR2, we discovered that the Ex-AMHR2 + AMH group exhibited significantly higher serum AMH levels than the In-AMHR2 + AMH group, along with hormonal profiles more consistent with PCOS pathology. Histological (H&E staining) analysis revealed severe follicular atresia, disorganized granulosa cell layers, and impaired luteal development in the Ex-AMHR2 + AMH group, further corroborated by reduced protein and mRNA expression of oocyte quality markers (GDF9, BMP15). Subsequent tissue-specific studies on AMHR2 reveal that the Neur-AMHR2−/−+AMH group demonstrated restored estrous cyclicity, improved serum levels of AMH and related hormones, compared with Ovary-AMHR2−/−+AMH group, indicating attenuated PCOS symptoms. Consistently, H&E staining and GDF9/BMP15 expression (protein & mRNA) confirmed enhanced oocyte quality in Neur-AMHR2−/− mice, reinforcing the central role of neuronal AMHR2 in mediating AMH-induced ovarian dysfunction.
conclusionNeuronal AMHR2 serves as the specific binding site for AMH, and the neuronal AMH/AMHR2 signaling pathway contributes to PCOS pathogenesis by disrupting HPO axis hormone secretion and interfering with cyclic follicular development. CLINICAL TRIAL NUMBER: Not applicable.
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