Follicular fluid (FF) plays a vital role in the bidirectional communication between oocytes and granulosa cells (GCs), regulating and promoting oocyte growth and development. This fluid constitutes a complex microenvironment, rich in various molecules including hormones, growth factors, cytokines, lipids, proteins, and extracellular vesicles. Understanding the composition and metabolic profile of follicular fluid is important for investigating ovarian pathologies such as polycystic ovary syndrome (PCOS) and endometriosis. Additionally, analyzing follicular fluid can offer valuable insights into oocyte quality, aiding in optimal oocyte selection for in vitro fertilization (IVF). This review provides an overview of follicular fluid composition, classification of its components and discusses the influential components of oocyte development. It also highlights the role of follicular fluid in the pathogenesis and diagnosis of ovarian diseases, along with potential follicular fluid biomarkers for assessing oocyte quality. By understanding the intricate relationship between follicular fluid and oocyte development, we can advance fertility research and improve clinical outcomes for infertility patients.

Over these years, more and more sex cord-stromal tumors have been reported. Granulosa cell tumor (GCT) is a rare tumor in ovaries, accounts for 2% to 5% of ovarian cancers. The main different feature of GCTs from other ovarian cancers is that GCTs can lead to abnormally secreted hormones (estrogen, inhibin and Müllerian inhibiting substance). The GCT is divided into two categories according to the age of patients, namely AGCT (adult granulosa cell tumor) and JGCT (Juvenile granulosa cell tumor). AGCT patients accounts for 95%. Although the pathogenesis is not clear, FOXL2 (Forkhead box L2) mutation was considered as the most critical factor in AGCT development. The current treatment is dominated by surgery. Target therapy remains in the adjuvant therapy stage, such as hormone therapy. During these years, other pathogenic factors were also explored, such as PI3K/AKT (phosphatidylinositol-3-kinase; serine/threonine kinase), TGF-β (Transforming growth factor beta) signaling pathway, Notch signaling pathway, GATA4 and VEGF (vascular endothelial growth factor). These factors and signaling pathway play important roles in GCT cell proliferation, apoptosis, or angiogenesis. The purpose of this review is to summarize the possible pathogenic factors and signaling pathways, which may shed lights on developing potential therapeutic targets for GCT.

Primary ovarian insufficiency (POI) is a heterogeneous disease resulting from non-functional ovaries in women before the age of 40. It is characterized by primary amenorrhea or secondary amenorrhea. As regards its etiology, although many POI cases are idiopathic, menopausal age is a heritable trait and genetic factors play an important role in all POI cases with known causes, accounting for approximately 20% to 25% of cases. This paper reviews the selected genetic causes implicated in POI and examines their pathogenic mechanisms to show the crucial role of genetic effects on POI. The genetic factors that can be found in POI cases include chromosomal abnormalities (e.g., X chromosomal aneuploidies, structural X chromosomal abnormalities, X-autosome translocations, and autosomal variations), single gene mutations (e.g., newborn ovary homeobox gene (NOBOX), folliculogenesis specific bHLH transcription factor (FIGLA), follicle-stimulating hormone receptor (FSHR), forkhead box L2 (FOXL2), bone morphogenetic protein 15 (BMP15), etc., as well as defects in mitochondrial functions and non-coding RNAs (small ncRNAs and long ncRNAs). These findings are beneficial for doctors to diagnose idiopathic POI cases and predict the risk of POI in women.

Premature ovarian insufficiency (POI) is an important cause of infertility and also cause menopausal symptoms, which greatly reduced the quality of life for women. Hormone replacement therapy (HRT), as an important strategy, improved the quality of life for patients, however, the role of HRT in promoting fertility remains controversial. Therefore, seeking an optimal regime for POI becomes more urgent. In this study, we established POI model induced by CTX and BUS and utilized bone marrow derived mesenchymal stem cells (BM-MSCs) transplantation to treat the POI. We found that the decrease of estrogen and the increase of FSH induced by administration of CTX and BUS were rescued by BM-MSC transplantation. H&E staining and TUNEL assay showed that there were more healthy ovarian follicles and less apoptosis of ovarian cells after treatment with BM-MSCs. Further studies showed that there was an obvious decrease of Bax, p53, and p21 after transplantation, however, CyclinD2 was increased. In conclusion, our results demonstrated that BM-MSCs could restore injured ovarian function. Inhibiting apoptosis and promoting residual ovarian cell proliferation may contribute to the process.