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Special Issue "Novel Physiology and Molecular Pathology of Reproduction, Novel Treatments of Infertility 2.0"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 October 2021).

Special Issue Editor

Prof. Dr. Micheline Misrahi
E-Mail Website
Guest Editor
Biochemistry and Molecular Biology Faculty of Medicine, University Paris-South Molecular Genetics of Reproductive and Metabolic Diseases Bicetre Hospital, Gif-sur-Yvette, France
Interests: molecular and cellular mechanisms in reproductive endocrinology; nuclear receptors; membrane receptors; gonadotropins and their receptors; thyrotropin receptor; reproductive genetics; genetics of male and female infertility; primary ovarian insufficiency; disorders of puberty; genetic diseases of GPCR
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Special Issue Information

Dear Colleagues,

Despite the major developments that have taken place in the field in the last few decades, infertility still poses a major diagnostic and therapeutic challenge, and overall, less than 50% of couples attending infertility treatments can be helped. About 1 out of 7 couples have difficulties to conceive, and the figure is bound to increase due to the demographic change with regard to the increase in maternal age when acquiring children. Very roughly, in about 1/3 of couples, the cause of infertility can be traced back to the female side, 1/3 to the male side, and in 1/3 of cases, the cause can be found in both. Primary ovarian insufficiency (POI) affects ~1% of women before they reach 40 years of age. The most frustrating cases are idiopathic (15–30% of couples), where no cause and no rational treatment can be offered. For these reasons, new information about the pathogenesis, diagnosis, and treatment of male and female infertility is urgently needed. This Special Issue aims to review recent research on male and female infertility. The recent leap in genetic knowledge obtained through next-generation sequencing (NGS) together with animal models has further elucidated their molecular pathogenesis, identifying novel genes/pathways. Mutations of >60 genes or more than 100 genes in isolated female and male infertility, respectively, emphasize the high genetic heterogeneity. NGS will provide a genetic diagnosis leading to genetic/therapeutic counseling. Defects in meiosis or DNA repair genes may predispose to tumors. Specific gene mutations may predict the risk of a rapid loss of a persistent ovarian reserve in women, an important determinant in fertility preservation. Novel physiology and newly identified regulators of ovarian folliculogenesis and ovulation will be developed. Novel mechanisms that regulate the activation of primordial follicles have been unraveled, and they lead to innovative treatments. Indeed, a recent treatment of POI by in vitro activation of dormant follicles (IVA) proved successful. Other innovative treatments are in development (e.g., stem cells). On the male side, the latest data on hormonal regulation of spermatogenesis, genetic and epigenetic approaches to addressing idiopathic failure of spermatogenesis, attempts to achieve in vitro spermatogenesis, the effect of general health on male fertility, and new treatment modalities and their outcome will be reviewed.

Prof. Dr. Micheline Misrahi
Guest Editor

Manuscript Submission Information

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Keywords

  • Spermatogenesis
  • Infertility
  • Hypothalamic–pituitary–gonadal axis
  • In vitro fertilization (IVF)
  • Intracytoplasmic sperm injection (ICVSI)
  • Hypogonadism
  • Primary ovarian insufficiency
  • Next generation sequencing
  • Meiosis
  • DNA repair
  • In vitro activation of dormant follicles (IVA)
  • Stem cells

Published Papers (2 papers)

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Research

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Article
Increased Systemic Antioxidant Power Ameliorates the Aging-Related Reduction in Oocyte Competence in Mice
Int. J. Mol. Sci. 2021, 22(23), 13019; https://doi.org/10.3390/ijms222313019 - 01 Dec 2021
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Abstract
Ovarian aging is associated with elevated oxidative stress and diminished oocyte developmental competence. We aimed to determine the impact of systemic antioxidant treatment in aged mice. Female outbred CF-1 mice were aged for 9 months prior to an 8-week 45 mg Euterpe oleracea [...] Read more.
Ovarian aging is associated with elevated oxidative stress and diminished oocyte developmental competence. We aimed to determine the impact of systemic antioxidant treatment in aged mice. Female outbred CF-1 mice were aged for 9 months prior to an 8-week 45 mg Euterpe oleracea (açaí) daily supplement. The açaí treatment induced a threefold increase in serum antioxidant power (FRAP) compared to both young and aged mice (p < 0.0001). Compared to young mice, aged mice had fewer oocytes and reduced blastocyst development (p < 0.0001); açaí did not affect the oocyte numbers, but improved blastocyst formation (p < 0.05). Additionally, açaí alleviated the aging-related decrease in implantation potential (p < 0.01). The aged mice showed evidence of elevated ovarian ER stress (increased whole-ovary PDIA4 expression, granulosa cell and oocyte GRP78 expression, and oocyte PDIA4 protein), reduced oocyte mitochondrial quality (higher PRKN activation and mitochondrial DNA oxidative damage), and dysregulated uterine glandular epithelium. Antioxidant intervention was sufficient to lessen these effects of ovarian aging, likely in part by the upregulation of NRF2. We conclude that açaí treatment is a promising strategy to improve ER and mitochondrial function in the ovaries, thereby ameliorating the decreased oocyte competence that occurs with ovarian aging. Full article
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Review

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Review
The Roles of Luteinizing Hormone, Follicle-Stimulating Hormone and Testosterone in Spermatogenesis and Folliculogenesis Revisited
Int. J. Mol. Sci. 2021, 22(23), 12735; https://doi.org/10.3390/ijms222312735 - 25 Nov 2021
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Abstract
Spermatogenesis and folliculogenesis involve cell–cell interactions and gene expression orchestrated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). FSH regulates the proliferation and maturation of germ cells independently and in combination with LH. In humans, the requirement for high intratesticular testosterone (T) concentration [...] Read more.
Spermatogenesis and folliculogenesis involve cell–cell interactions and gene expression orchestrated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). FSH regulates the proliferation and maturation of germ cells independently and in combination with LH. In humans, the requirement for high intratesticular testosterone (T) concentration in spermatogenesis remains both a dogma and an enigma, as it greatly exceeds the requirement for androgen receptor (AR) activation. Several data have challenged this dogma. Here we report our findings on a man with mutant LH beta subunit (LHβ) that markedly reduced T production to 1–2% of normal., but despite this minimal LH stimulation, T production by scarce mature Leydig cells was sufficient to initiate and maintain complete spermatogenesis. Also, in the LH receptor (LHR) knockout (LuRKO) mice, low-dose T supplementation was able to maintain spermatogenesis. In addition, in antiandrogen-treated LuRKO mice, devoid of T action, the transgenic expression of a constitutively activating follicle stimulating hormone receptor (FSHR) mutant was able to rescue spermatogenesis and fertility. Based on rodent models, it is believed that gonadotropin-dependent follicular growth begins at the antral stage, but models of FSHR inactivation in women contradict this claim. The complete loss of FSHR function results in the complete early blockage of folliculogenesis at the primary stage, with a high density of follicles of the prepubertal type. These results should prompt the reassessment of the role of gonadotropins in spermatogenesis, folliculogenesis and therapeutic applications in human hypogonadism and infertility. Full article
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