Decreased oocyte quality in patients with endometriosis is closely related to abnormal granulosa cells

Abstract

Infertility and menstrual abnormalities in endometriosis patients are frequently caused by aberrant follicular growth or a reduced ovarian reserve. Endometriosis typically does not directly harm the oocyte, but rather inhibits the function of granulosa cells, resulting in a decrease in oocyte quality. Granulosa cells, as oocyte nanny cells, can regulate meiosis, provide the most basic resources required for oocyte development, and influence ovulation. Endometriosis affects oocyte development and quality by causing granulosa cells apoptosis, inflammation, oxidative stress, steroid synthesis obstacle, and aberrant mitochondrial energy metabolism. These aberrant states frequently interact with one another, however there is currently relatively little research in this field to understand the mechanism of linkage between abnormal states.

Methyl 3,4-dihydroxybenzoate alleviates oxidative damage in granulosa cells by activating Nrf2 antioxidant pathway

“…Oxidative stress induced apoptosis is a key pathogenesis of many diseases. Previous studies have shown that oxidative stress in the follicular microenvironment is an important factor that leads to infertility in endometriosis and has been speculated to hamper GCs function, folliculogenesis, and oocyte maturation [ 24 ]. Oxidative damage induced GCs apoptosis was considered as a significant cause of compromised follicle quality and adverse outcomes of assisted reproductive technology (ART) in endometriosis [ 25 ].…”

Knockdown of DNMT1 Induces SLCO3A1 to Promote Follicular Growth by Enhancing the Proliferation of Granulosa Cells in Mammals

“…In recent years, the incidence of female reproductive disorders, such as PCOS, endometriosis, and diminished ovarian reserve, have been increasing, which is a serious threat to women’s health and fertility [ 25 ]. Follicular growth can be delayed due to a decreased proliferation of GCs and increased apoptosis of GCs, which are thought to play essential roles in the pathogenesis of female reproductive diseases [ 5 , 26 , 27 ]. However, there is no effective therapy for these disorders, and the specific mechanisms regulating follicular growth remain to be further explored.…”

“…As the basic functional unit of ovaries [ 1 ], the normal growth, development and ovulation of follicles are necessary for the generations of mammals [ 2 ]. In humans , a series of female reproductive diseases such as polycystic ovary syndrome (PCOS) [ 3 , 4 ], endometriosis [ 5 ], and dysfunction of ovarian reserve [ 6 ] present the clinical feature of abnormal follicular growth. However, no effective therapy treats and cures these devastating diseases.…”

Immune and oxidative stress disorder in ovulation-dysfunction women revealed by single-cell transcriptome

“…In our study, we observed a consistent reduction in the expression of oxidative stress-related genes, including JUN and FOS , in almost all cellular clusters of peripheral blood mononuclear cells (PBMCs). Given that granulosa cells serve as the energy source for oocytes, abnormal levels of oxidative stress can affect oocyte development, potentially leading to ovulation disorders ( 36 , 37 ). Supplementing our findings with transcriptome data derived from the ovaries of high-fat diet-induced mice and aging monkeys, we identified a concurrent upregulation of oxidative stress-related genes, specifically NDUFV3 , NDUFB6 , NFE2L2 , PARK7 , and GPX7 ( 24 ), in both granulosa cells and PBMCs of women suffering from ovulatory disorders.…”