Department of Obstetrics and Gynecology, Faculty of Medical Sciences, University of Fukui, Fukui, Japan.
Department of Nursing, Faculty of Nursing and Welfare Sciences, Fukui Prefectural University, Fukui, Japan.
Front Endocrinol (Lausanne). 2023 Dec 13;14:1324429. doi: 10.3389/fendo.2023.1324429. eCollection 2023.
The ovarian microenvironment is critical for follicular development and oocyte maturation. Maternal conditions, including polycystic ovary syndrome (PCOS), endometriosis, and aging, may compromise the ovarian microenvironment, follicular development, and oocyte quality. Chronic low-grade inflammation can induce oxidative stress and tissue fibrosis in the ovary. In PCOS, endometriosis, and aging, pro-inflammatory cytokine levels are often elevated in follicular fluids. In women with obesity and PCOS, hyperandrogenemia and insulin resistance induce ovarian chronic low-grade inflammation, thereby disrupting follicular development by increasing oxidative stress. In endometriosis, ovarian endometrioma-derived iron overload can induce chronic inflammation and oxidative stress, leading to ovarian ferroptosis and fibrosis. In inflammatory aging (inflammaging), senescent cells may secrete senescence-associated secretory phenotype factors, causing chronic inflammation and oxidative stress in the ovary. Therefore, controlling chronic low-grade inflammation and fibrosis in the ovary would present a novel therapeutic strategy for improving the follicular microenvironment and minimizing ovarian dysfunction.
卵巢微环境对卵泡发育和卵母细胞成熟至关重要。母体状况,包括多囊卵巢综合征(PCOS)、子宫内膜异位症和衰老,可能会损害卵巢微环境、卵泡发育和卵母细胞质量。慢性低度炎症可在卵巢中诱导氧化应激和组织纤维化。在 PCOS、子宫内膜异位症和衰老中,卵泡液中的促炎细胞因子水平常常升高。在肥胖和 PCOS 的女性中,高雄激素血症和胰岛素抵抗会诱导卵巢慢性低度炎症,从而通过增加氧化应激来破坏卵泡发育。在子宫内膜异位症中,卵巢子宫内膜异位症来源的铁过载可诱导慢性炎症和氧化应激,导致卵巢铁死亡和纤维化。在炎症性衰老(炎症衰老)中,衰老细胞可能会分泌衰老相关分泌表型因子,导致卵巢慢性炎症和氧化应激。因此,控制卵巢中的慢性低度炎症和纤维化将为改善卵泡微环境和最小化卵巢功能障碍提供一种新的治疗策略。