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卵巢纤维化:分子机制与潜在治疗靶点。

Ovarian fibrosis: molecular mechanisms and potential therapeutic targets.

机构信息

State Key Laboratory of Female Fertility Promotion, Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China.

Key Laboratory of Assisted Reproduction (Peking University), Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Ministry of Education, Beijing, 100191, China.

出版信息

J Ovarian Res. 2024 Jul 5;17(1):139. doi: 10.1186/s13048-024-01448-7.

Abstract

Ovarian fibrosis, characterized by the excessive proliferation of ovarian fibroblasts and the accumulation of extracellular matrix (ECM), serves as one of the primary causes of ovarian dysfunction. Despite the critical role of ovarian fibrosis in maintaining the normal physiological function of the mammalian ovaries, research on this condition has been greatly underestimated, which leads to a lack of clinical treatment options for ovarian dysfunction caused by fibrosis. This review synthesizes recent research on the molecular mechanisms of ovarian fibrosis, encompassing TGF-β, extracellular matrix, inflammation, and other profibrotic factors contributing to abnormal ovarian fibrosis. Additionally, we summarize current treatment approaches for ovarian dysfunction targeting ovarian fibrosis, including antifibrotic drugs, stem cell transplantation, and exosomal therapies. The purpose of this review is to summarize the research progress on ovarian fibrosis and to propose potential therapeutic strategies targeting ovarian fibrosis for the treatment of ovarian dysfunction.

摘要

卵巢纤维化的特征是卵巢成纤维细胞的过度增殖和细胞外基质(ECM)的积累,是卵巢功能障碍的主要原因之一。尽管卵巢纤维化在维持哺乳动物卵巢的正常生理功能方面起着至关重要的作用,但对这种疾病的研究却被大大低估了,这导致了针对纤维化引起的卵巢功能障碍缺乏临床治疗选择。本综述综合了最近关于卵巢纤维化分子机制的研究,包括 TGF-β、细胞外基质、炎症和其他促纤维化因素对异常卵巢纤维化的影响。此外,我们还总结了目前针对卵巢纤维化的卵巢功能障碍治疗方法,包括抗纤维化药物、干细胞移植和外泌体治疗。本综述的目的是总结卵巢纤维化的研究进展,并提出针对卵巢纤维化的潜在治疗策略,以治疗卵巢功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/651b/11225137/ecc4c5f3ae2e/13048_2024_1448_Fig1_HTML.jpg

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