Decreased neurotensin induces ovulatory dysfunction via the NTSR1/ERK/EGR1 axis in polycystic ovary syndrome
Peer-Reviewed Publication
Updates every hour. Last Updated: 9-Jun-2025 22:09 ET (10-Jun-2025 02:09 GMT/UTC)
Polycystic ovary syndrome (PCOS) represents a significant health concern for women of reproductive age, manifesting as a complex endocrine disorder with diverse clinical presentations. Characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology, PCOS affects 5% to 20% of women and stands as a leading cause of anovulatory infertility. The pathophysiology of PCOS involves abnormal folliculogenesis, resulting in arrested follicular development and the accumulation of small antral follicles. This follicular arrest is accompanied by mitochondrial dysfunction and oxidative stress, contributing to poor oocyte quality and developmental potential. Recent research has highlighted the potential role of neurotensin (NTS), a gut-brain peptide, in the regulation of ovulation and its dysfunction in PCOS.
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