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Objective： Ovarian fibrosis is characterized by excessive proliferation of ovarian fibroblasts and deposition ofextracellular matrix （ECM） and it is one of the principal reasons for ovarian dysfunction. This review aimed to investigate the pathogenetic mechanism of ovarian fibrosis and to clarify the relationship between ovarian diseases and fibrosis. Data Sources： We searched PubMed for English language articles published up to November 2016. The search terms included ovarian fibrosis OR fibrosis, ovarian chocolate cyst OR ovarian endometrioma, polycystic ovarian syndrome （PCOS）, premature ovarian failure, ECM, matrix rnetalloproteinases （MMPs）, tissue inhibitors of matrix metalloproteinases （TIMPs）, transforming growth factor-beta 1 （TGF-[31）, connective tissue growth factor （CTGF）, peroxisome proliferator-activated receptor gamma （PPAR-T）, vascular endothelial growth factor （VEGF）, endothelin-1 （ET-1）, and combinations of these terms. Study Selection： Articles were obtained and reviewed to analyze the pathogenic mechanism of ovarian fibrosis and related ovarian diseases. Results： Many cytokines, such as MMPs, TIMPs, TGF-β1, CTGF, PPAR-γ, VEGK and ET- 1, are involved in ovarian fibrogenesis. Ovarian fibrogenesis is associated with various ovarian diseases, including ovarian chocolate cyst PCOS, and premature ovarian failure. One finding of particular interest is that fibrogenesis in peripheral tissues around an ovarian chocolate cyst commonly causes ovarian function diminution, and therefore, this medical problem should arouse widespread concern in clinicians worldwide. Conclusions： Patients with ovarian fibrosis are susceptible to infertility and tend to have decreased responses to assisted fertility treatment. Thus, protection of ovarian function should be a priority for women who wish to reproduce when making therapeutic decisions about ovarian fibrosis-related diseases.

Premature ovarian failure (POF) syndrome, an early decline of ovarian function in women, is frequently associated with X chromosome abnormalities ranging from various Xq deletions to complete loss of one of the X chromosomes. However, the genetic locus responsible for the POF remains unknown, and no candidate gene has been identified. Using the Cre/LoxP system, we have disrupted the mouse X chromosome androgen receptor (Ar) gene. Female$AR^{-/-}$mice appeared normal but developed the POF phenotype with aberrant ovarian gene expression. Eight-week-old female$AR^{-/-}$mice are fertile, but they have lower follicle numbers and impaired mammary development, and they produce only half of the normal number of pups per litter. Forty-week-old$AR^{-/-}$mice are infertile because of complete loss of follicles. Genome-wide microarray analysis of mRNA from$AR^{-/-}$ovaries revealed that a number of major regulators of folliculogenesis were under transcriptional control by AR. Our findings suggest that AR function is required for normal female reproduction, particularly folliculogenesis, and that AR is a potential therapeutic target in POF syndrome.

Fragile X and fragile X-associated tremor-ataxia syndrome (FXTAS) are caused by mutations of the FMR1 gene. The mutations causing FXTAS can expand in a generation to a “full mutation” causing fragile X syndrome. The mutations causing FXTAS and the phenotype, fragile X-associated premature ovarian insufficiency (FXPOI), are referred to as the FMR1 premutation (PM). The objective of this paper was to formulate a theory to explain the Mechanism for FXPOI.Recent research on fragile X syndrome and FXTAS has led to sophisticated theories about the mechanisms underlying these diseases. It has been proposed that similar mechanisms underlie FXPOI. Utilizing recent research on FXTAS, but a more detailed application of ovarian physiology, we present a more ovarian specific theory as to the primary mechanism explaining the development of FXPOI.The FXPOI phenotype may best be viewed as derivative of the observation that fragile X PM carriers experience menopause an average of 5 years earlier than non-carriers. Women carrying the PM experience an earlier menopause because of an accelerated activation of their primordial follicle pool. This acceleration of primordial follicle activation occurs, in part, because of diminished AMH production. AMH production is diminished because of accelerated atresia of early antral follicles. This accelerated atresia likely occurs because the fragile X PM leads to a slowing of the rate of granulosa cell mitosis in some follicles.

Background: Premature ovarian failure (POF), is menopause occurring before the age of 40, affecting 1-3% of women worldwide. The risk of POF increases with altered immunological parameters such as FAS and FASL genes, which play a fundamental role in embryogenesis and cellular homeostasis. Objective: The study aimed to investigate the potential role of FAS and FASL genes in POF pathogenesis. Materials and Methods: In this case-control study, the polymorphisms of FAS-670A/G and FASLIVS2nt_124A/G apoptotic genes were analyzed in 51 Iranian women suffering from POF, and 61 healthy controls. Isolation of DNA was done using the salting-out method, and genotypic analysis was performed for all the subjects using the polymerase chain reaction-restriction fragment length polymorphism method. Results: Our results revealed that homozygous FAS-670A/A and G/G, and heterozygous FAS-670A/G are not significantly different between cases and controls (p = 0.99). Also, in different genotyping models of FASIVS2nt_124, polymorphisms were not related to POF risk (p = 0.23). Conclusion: There is no statistical association between these polymorphisms and POF risk in women referred to genetic counseling clinics. Key words: FAS, FASL, Polymorphism, Premature ovarian failure.

Background: Premature ovarian failure (POF) is a disease that affects female fertility but has few effective treatments. Ovarian reserve function plays an important role in female fertility. Recent studies have reported that hydrogen can protect male fertility. Therefore, we explored the potential protective effect of hydrogen-rich water on ovarian reserve function through a mouse immune POF model. Methods: To set up immune POF model, fifty female BALB/c mice were randomly divided into four groups: Control (mice consumed normal water, n = 10), hydrogen (mice consumed hydrogen-rich water, n = 10), model (mice were immunized with zona pellucida glycoprotein 3 [ZP3] and consumed normal water, n = 15), and model-hydrogen (mice were immunized with ZP3 and consumed hydrogen-rich water, n = 15) groups. After 5 weeks, mice were sacrificed. Serum anti-Müllerian hormone (AMH) levels, granulosa cell (GC) apoptotic index (AI), B-cell leukemia/lymphoma 2 (Bcl-2), and BCL2-associated X protein (Bax) expression were examined. Analyses were performed using SPSS 17.0 (SPSS Inc., Chicago, IL, USA) software. Results: Immune POF model, model group exhibited markedly reduced serum AMH levels compared with those of the control group (5.41 ± 0.91 ng/ml vs. 16.23 ± 1.97 ng/ml, P = 0.033) and the hydrogen group (19.65 ± 7.82 ng/ml, P = 0.006). The model-hydrogen group displayed significantly higher AMH concentrations compared with that of the model group (15.03 ± 2.75 ng/ml vs. 5.41 ± 0.91 ng/ml, P = 0.021). The GC AI was significantly higher in the model group (21.30 ± 1.74%) than those in the control (7.06 ± 0.27%), hydrogen (5.17 ± 0.41%), and model-hydrogen groups (11.24 ± 0.58%) (all P < 0.001). The GC AI was significantly higher in the model-hydrogen group compared with that of the hydrogen group (11.24 ± 0.58% vs. 5.17 ± 0.41%, P = 0.021). Compared with those of the model group, ovarian tissue Bcl-2 levels increased (2.18 ± 0.30 vs. 3.01 ± 0.33, P = 0.045) and the Bax/Bcl-2 ratio decreased in the model-hydrogen group. Conclusions: Hydrogen-rich water may improve serum AMH levels and reduce ovarian GC apoptosis in a mouse immune POF model induced by ZP3.

There are large variations in the number of oocytes within each woman, and biologically, the total quantity is at its maximum before the woman is born. Scientific knowledge is limited about factors controlling the oocyte pool and how to measure it. Within fertility clinics, there is no uniform agreement on the diagnostic criteria for each common measure of ovarian reserve in women, and thus, studies often conflict. While declining oocyte quantity/quality is a normal physiologic occurrence as women age, some women experience diminished ovarian reserve (DOR) much earlier than usual and become prematurely infertile. Key clinical features of DOR are the presence of regular menstrual periods and abnormal-but-not-postmenopausal ovarian reserve test results. A common clinical challenge is counseling patients with conflicting ovarian reserve test results. The clinical diagnosis of DOR and the interpretation of ovarian reserve testing are complicated by changing lab testing options and processing for anti-mullerian hormone since 2010. Further, complicating the diagnostic and research scenario is the existence of other distinct yet related clinical terms, specifically premature ovarian failure, primary ovarian insufficiency, poor ovarian response, and functional ovarian reserve. The similarities and differences between the definitions of DOR with each of these four terms are reviewed. We recommend greater medical community involvement in terminology decisions, and the addition of DOR-specific medical subject-heading search terms.

Premature ovarian insufficiency (POI) is the loss of normal ovarian function before the age of 40 years, a condition that affects approximately 1% of women under 40 years old and 0.1% of women under 30 years old. It is biochemically characterized by amenorrhea with hypoestrogenic and hypergonadotropic conditions, in some cases, causing loss of fertility. Heterogeneity of POI is registered by genetic and non-genetic causes, such as autoimmunity, environmental toxins, and chemicals. The identification of possible causative genes and selection of candidate genes for POI confirmation remain to be elucidated in cases of idiopathic POI. This review discusses the current understanding and future prospects of heterogeneous POI. We focus on the genetic basis of POI and the recent studies on non-coding RNA in POI pathogenesis as well as on animal models of POI pathogenesis, which help unravel POI mechanisms and potential targets. Despite the latest discoveries, the crosstalk among gene regulatory networks and the possible therapies targeting the same needs to explore in near future.

About 10% of women of reproductive age are unable to conceive or carry a pregnancy to term. Female factors alone account for at least 35% of all infertility cases and comprise a wide range of causes affecting ovarian development, maturation of oocytes, and fertilization competence, as well as the potential of a fertilized egg for preimplantation development, implantation, and fetal growth. Genetic abnormalities leading to infertility in females comprise large chromosome abnormalities, submicroscopic chromosome deletion and duplications, and DNA sequence variations in the genes that control numerous biological processes implicated in oogenesis, maintenance of ovarian reserve, hormonal signaling, and anatomical and functional development of female reproductive organs. Despite the great number of genes implicated in reproductive physiology by the study of animal models, only a subset of these genes is associated with human infertility. In this review, we mainly focus on genetic alterations identified in humans and summarize recent knowledge on the molecular pathways of oocyte development and maturation, the crucial role of maternal-effect factors during embryogenesis, and genetic conditions associated with ovarian dysgenesis, primary ovarian insufficiency, early embryonic lethality, and infertility.

Granulosa cells are essential for follicle initiation and development, and their abnormal function or apoptosis is a crucial factor leading to follicular atresia. A state of oxidative stress occurs when the balance between the production of reactive oxygen species and the regulation of the antioxidant system is disturbed. Oxidative stress is one of the most important causes of the abnormal function and apoptosis of granulosa cells. Oxidative stress in granulosa cells causes female reproductive system diseases, such as polycystic ovary syndrome and premature ovarian failure. In recent years, studies have confirmed that the mechanism of oxidative stress in granulosa cells is closely linked to the PI3K-AKT signaling pathway, MAPK signaling pathway, FOXO axis, Nrf2 pathway, NF-κB signaling pathway, and mitophagy. It has been found that drugs such as sulforaphane, Periplaneta americana peptide, and resveratrol can mitigate the functional damage caused by oxidative stress on granulosa cells. This paper reviews some of the mechanisms involved in oxidative stress in granulosa cells and describes the mechanisms underlying the pharmacological treatment of oxidative stress in granulosa cells.

Premature ovarian failure (POF) is the term usually used to describe women aged younger than 40 years, who present with amenorrhoea, hypergonadotropic hypogonadism, and infertility. POF is a devastating diagnosis for reproductive-aged women. The clinical presentation is diverse, and several different disorders can lead to premature ovarian failure. POF has serious health consequences, including psychological distress, infertility, osteoporosis, autoimmune disorders, ischaemic heart disease, and increased risk of mortality. Hashimoto's disease is the most frequent autoimmune disorder associated with premature ovarian failure. Management should be initiated immediately to prevent long-term consequences. Oestrogen therapy is the mainstay of management. Hormone therapy should be provided to eliminate symptoms of oestrogen deficiency.