MiR-122-5p, high expression in follicular fluid exosomes of patients with endometriosis, impairs the glucose metabolism function of cumulus cells and may further impair oocyte quality. Endometriosis (EMs) affects fertility in women of childbearing age in many ways. However, the mechanisms are complex, including the decrease in oocyte quality, which still needs to be studied. Exosomes, small vesicles responsible for intercellular information exchange, have been found to be involved in many biological events, such as follicle development and oocyte meiosis recovery. From the perspective of follicular fluid exosomes, this study aims to elucidate the mechanism of EMs-related oocyte quality decline. Follicular fluid was collected from three groups of women: the untreated EMs group (EMs_UT), the satisfactorily treated EMs group (EMs_ST) and the control group (Ctrl). Mouse cumulus oocyte complexes (COCs) were cocultured with exosomes extracted from follicular fluid during in vitro maturation. Oocyte quality and cumulus cell function were assessed. High-throughput sequencing of miRNA in exosomes was conducted. The function of differentially expressed miRNAs was studied by using SVOG cells (human ovarian granulosa cell line) transfected with miRNA mimic and inhibitor. Our date suggest that follicular fluid exosomes from patients with untreated EMs reduce the maturation rate and damage the quality of mouse oocytes. MiR-122-5p, overexpressed in untreated EMs, inhibits the translation of key aldolase enzymes related to glucose metabolism and partially impairs cumulus cells of endometriosis patients.