Abstract
Kisspeptins are a family of neuropeptides that are critical for initiating puberty and regulating ovulation in sexually mature females via the central control of the hypothalamic–pituitary–gonadal axis. Recent studies have shown that kisspeptin and its receptor kisspeptin receptor (KISS1R) are expressed in the mammalian ovary. Convincing evidence indicates that kisspeptins can activate a wide variety of signals via its binding to KISS1R. Experimental data gathered recently suggest a putative role of kisspeptin signaling in the direct control of ovarian function, including follicular development, oocyte maturation, steroidogenesis, and ovulation. Dysregulation or naturally occurring mutations of the kisspeptin/KISS1R system may negatively affect the ovarian function, leading to reproductive pathology or female infertility. A comprehensive understanding of the expression, actions, and underlying molecular mechanisms of this system in the human ovary is essential for novel approaches to therapeutic and diagnostic interventions in reproductive diseases and infertility.
Highlights
Female reproduction is a highly orchestrated and regulated process controlled by the hypothalamic– pituitary–ovarian (HPO) axis
Consistent with these results, immature ovaries showed low to negligible levels of Kiss1 mRNA, which were significantly enhanced by gonadotropin priming [17]. All these findings strongly suggest that functional role of kisspeptin in regulating follicular development mainly occurs after puberty, which is in consistence with the age-related expression of kisspeptin in the ovary [17, 32, 39]
Emerging evidence indicates that the intraovarian kisspeptin/KISS1R system is of great importance in controlling female reproduction, including follicular development, oocyte maturation, steroidogenesis, and ovulation
Summary
Female reproduction is a highly orchestrated and regulated process controlled by the hypothalamic– pituitary–ovarian (HPO) axis. The pulsatile gonadotropin-releasing hormone (GnRH), and gonadotropins (FSH and LH), secretion primarily governs the HPO axis at puberty and maintains the cyclic function in adulthood [1]. This tonic GnRH/gonadotropins secretion is modulated by a negative feedback effect of serum estrogen secreted from the growing ovarian follicles [2]. Even though the critical role of GnRH in regulating female reproduction, there exist several functional limitations of the GnRH neuronal network. The major issue is that GnRH neurons do not express estrogen receptor α, the principle receptor that mediates both negative and positive estrogen feedback actions [5]
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