Abstract
Mammalian target of rapamycin (mTOR) is a conserved serine/threonine kinase of the phosphatidylinositol kinase-related kinase family that regulates cell growth, metabolism, and autophagy. Extensive research has linked mTOR to several human diseases including cancer, neurodegenerative disorders, and aging. In this review, recent publications regarding the mechanisms underlying the role of mTOR in female reproduction under physiological and pathological conditions are summarized. Moreover, we assess whether strategies to improve or suppress mTOR expression could have therapeutic potential for reproductive diseases like premature ovarian failure, polycystic ovarian syndrome, and endometriosis.
Highlights
Rapamycin is a macrocyclic lactone produced by the bacterium Streptomyces hygroscopicus that was previously used as an antifungal agent but abandoned soon after because of its immunosuppressive effect [1, 2]
The protein target of rapamycin (TOR) was originally discovered in genetic mutation studies using Saccharomyces cerevisiae [3] and subsequently found to be the target of the rapamycin–FKBP12 complex in mammalian cells, which is referred to as the mammalian target of rapamycin [4,5,6]. mTOR is sensitive to diverse environmental inputs including nutrients and growth factors, and regulates various fundamental cell processes including cell growth, metabolism, differentiation, and autophagy [7]
Activation of mTOR signaling in granulosa cells promotes follicular development as follicle stimulate hormone (FSH)-stimulated differentiation of GCs is necessary for follicular growth [62, 63]
Summary
Rapamycin is a macrocyclic lactone produced by the bacterium Streptomyces hygroscopicus that was previously used as an antifungal agent but abandoned soon after because of its immunosuppressive effect [1, 2]. Accumulating lines of evidence have shown that mTOR-regulated processes are important for folliculogenesis [13], oocyte meiotic maturation [14], ovarian somatic cell proliferation and steroidogenesis [15], puberty onset [16], ovarian aging [17], endometrium changes [18], and embryonic development [19]. Primordial follicle activation, which is the beginning of follicular development after puberty, determines ovarian reserve and reproductive lifespan [44].
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