Topic
Premature ovarian failure
About: Premature ovarian failure is a research topic. Over the lifetime, 2066 publications have been published within this topic receiving 69404 citations.
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TL;DR: The findings suggest that cryopreservation of ovarian tissue should be offered to all young women diagnosed with cancer and a livebirth after orthotopic autotransplantation of Cryopreserved ovarian tissue is described.
1,449 citations
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TL;DR: To assess the occurrence of premature ovarian failure, the age-specific incidence rates of natural menopause were determined for a cohort of 1858 women born between 1928 and 1932, and the incidence increased greatly in the age group 40 to 44.
965 citations
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TL;DR: It is shown that Foxo3a–/– female mice exhibit a distinctive ovarian phenotype of global follicular activation leading to oocyte death, early depletion of functional ovarian follicles, and secondary infertility, raising the possibility that accelerated follicular initiation plays a role in premature ovarian failure, a common cause of infertility and premature aging in women.
Abstract: Foxo transcription factors have been implicated in diverse biological processes, including metabolism, cellular stress responses, and aging Here, we show that Foxo3a-/- female mice exhibit a distinctive ovarian phenotype of global follicular activation leading to oocyte death, early depletion of functional ovarian follicles, and secondary infertility Foxo3a thus functions at the earliest stages of follicular growth as a suppressor of follicular activation In addition to providing a molecular entry point for studying the regulation of follicular growth, these results raise the possibility that accelerated follicular initiation plays a role in premature ovarian failure, a common cause of infertility and premature aging in women
812 citations
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TL;DR: Most women with POF are deeply upset by the diagnosis, partly due to the unexpected menopausal symptoms, but also due to infertility, and early detection would provide better opportunity for early intervention.
Abstract: Premature ovarian failure (POF) is a common cause of infertility in women, and is characterised by amenorrhoea, hypo-oestrogenism and elevated gonadotrophin levels in women under the age of 40. Known causes include iatrogenic agents that cause permanent damage to the ovaries, such as chemotherapy, radiation therapy and surgery, autoimmune conditions, X-chromosome abnormalities and autosomal genetic conditions. However, few genes have been identified that can explain a substantial proportion of cases of POF. Most women with POF are deeply upset by the diagnosis, partly due to the unexpected menopausal symptoms, but also due to infertility. Therefore, early detection would provide better opportunity for early intervention, and furthermore, the identification of specific gene defects will help to direct potential targets for future treatment.
696 citations
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TL;DR: It is shown that the murine Foxl2 gene is essential for granulosa cell differentiation and ovary maintenance, and it is suggested that granULosa cell function is not only crucial for oocyte growth but also to maintain follicular quiescence in vivo.
Abstract: Human Blepharophimosis/ptosis/epicanthus inversus syndrome (BPES) type I is
an autosomal dominant disorder associated with premature ovarian failure (POF)
caused by mutations in FOXL2 , a winged-helix/forkhead domain
transcription factor. Although it has been shown that FOXL2 is
expressed in adult ovaries, its function during folliculogenesis is not known.
Here, we show that the murine Foxl2 gene is essential for granulosa
cell differentiation and ovary maintenance. In
Foxl2 lacZ homozygous mutant ovaries granulosa
cells do not complete the squamous to cuboidal transition leading to the
absence of secondary follicles and oocyte atresia. We further demonstrate that
activin-βA and anti-Mullerian inhibiting hormone expression is absent or
strongly diminished in Foxl2 lacZ homozygous
mutant ovaries. Unexpectedly, two weeks after birth most if not all oocytes
expressed Gdf9 in Foxl2 lacZ homozygous
mutant ovaries, indicating that nearly all primordial follicles have already
initiated folliculogenesis at this stage. This activation, in the absence of
functional granulosa cells, leads to oocyte atresia and progressive follicular
depletion. In addition to providing a molecular mechanism for premature
ovarian failure in BPES, these results suggest that granulosa cell function is
not only crucial for oocyte growth but also to maintain follicular quiescence
in vivo.
658 citations