Abstract:

Oocyte senescence is the core link of fertility decline in older women. Studies have found that the decline of oocyte quality is related to the disturbance of ovarian immune microenvironment in ageing women. Imbalanced proportions of immune cells such as macrophages and T lymphocytes disrupts the immune homeostasis and drives ovarian fibrosis. The overexpression of inflammatory factors and inflammasomes directly destroys the spindle structure of oocytes and interferes with meiosis. The local chronic inflammation mediated by senescence-associated secretory phenotype (SASP) disrupts the local immune homeostasis of ovary. Mitochondrial dysfunction leads to dysfunction of immune axis, and ferroptosis activates a new type of ovarian immunosenescence, which is closely related to the synergistic regulatory effects. By destroying the oocyte skeleton, reducing meiosis ability, exacerbating oxidative stress and inducing apoptosis, these disorders directly or indirectly lead to the decline of oocyte quality and the impairment of embryonic development potential. This paper reviews the mechanisms of age-related oocyte quality decline from the perspective of immunology, and provides a reference for the subsequent development of fertility improvement strategies targeting the ovarian immune microenvironment.

Key words: Oocytes, Aging, Immunity, Senescence-associated secretion phenotype, Ferroptosis