ArticleJournal of ovarian research2026
The BDNF/TrkB/CREB signaling improves chronic stress-induced decreased ovarian reserve by inhibiting pyroptosis of granulosa cells and disorders of sex hormone secretion.
Article in Journal of ovarian research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDecreased ovarian reserve (DOR) seriously affects female reproductive health. However, the mechanism of DOR remains unknown. This study aimed to explore the mechanism of BDNF/TrkB/CREB signaling in granulosa cell pyroptosis and sex hormone secretion in DOR.
methodsRecombinant BDNF (rBDNF) and TrkB antagonist ANA-12 were used to investigate the effects of the BDNF-TrkB signaling pathway on chronic unpredictable stress (CUS)-induced DOR in vivo. The mechanism of the BDNF-TrkB signaling pathway in NE-induced pyroptosis and sex hormone secretion was further investigated in vitro by the combined application of the CREB antagonist KG-501.
resultsThe CUS model reduced BDNF expression in brain tissue, peripheral blood, and ovarian tissues and inhibited p-TrkB/TrkB, p-PI3K/PI3K, and p-AKT/AKT expression. rBDNF enhanced the ovarian index and improved histological structure in CUS mice, restored the disordered estrus cycle, reduced the serum corticosterone level, and increased the pregnancy rate and embryo number. rBDNF inhibited serum FSH, LH, and NE levels and apoptosis in CUS mice while increasing AMH, E
conclusionOur findings indicate that the BDNF-TrkB signaling pathway inhibits pyroptosis of granulosa cells and sex hormone secretion disorders by promoting CREB phosphorylation, thereby improving DOR. These results provide a new theoretical basis in DOR for targeting the BDNF-TrkB-CREB axis.
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