No abstract

the conversion of androgens to estrogens and progesterone synthesis [7]. Sadigh and others reported that the apoptotic and inflammation in the GC were related to the follicle, and the ovarian follicular growth was usually arrested in PCOS [8,9]. A clinical study reported that oxidative stress can induce the apoptosis of GCs in PCOS patients via the phosphoinositide 3-kinases/protein kinase B (PI3K/Akt) pathway [10]. Additional studies have demonstrated increased proliferation of GCs in the ovaries of anovulatory women compared to normal ovulatory women with PCOS [11]. Similarly, Ji found that the AT-rich interaction domain 1A (ARID1A) is downregulated in GC cells from women and in mouse models with PCOS, and the ARID1A overexpression can inhibit the PI3K/Akt pathway to