中医药调控PI3K/AKT通路改善卵巢储备功能减退的研究进展
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18775288819

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全国名中医陈慧侬学术思想与临床诊疗传承发展推广中心建设项目(桂中医大党委[2022]23号)


Research Progress on the Mechanism of Traditional Chinese Medicine in Improving Diminished Ovarian Reserve Function by Regulating the PI3K/AKT Signaling Pathway
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18775288819

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    摘要:

    卵巢储备功能减退(Diminished ovarian reserve,DOR)是指卵巢内卵母细胞数量减少、质量下降,是一种复杂的妇科疾病,影响着全球数百万女性,经常导致月经紊乱和不孕不育。随着婚育年龄的后延,DOR成为影响女性生育能力的一个重要因素。本文归纳了DOR发生发展涉及的多种发病机制及信号通路,其中磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/AKT)信号通路在卵巢功能调控中发挥着核心作用。本文表明PI3K/AKT通路在DOR的发病中具有重要作用,该通路可以通过调控颗粒细胞凋亡、调节卵巢炎症反应、调节颗粒细胞及卵泡细胞的自噬以及氧化应激等过程,在DOR发生发展中发挥作用。本文重点总结了PI3K/AKT通路与DOR发生机制之间的密切关联,以及综述了最新关于中药单体及复方通过该通路治疗DOR的实验研究,为治疗DOR研究的深入开展提供借鉴。

    Abstract:

    Diminished Ovarian Reserve (DOR) refers to a complex gynecological disorder characterized by reduced quantity and impaired quality of oocytes in the ovaries. It affects millions of women worldwide, often leading to menstrual irregularities and infertility. With the delayed age of marriage and childbearing, DOR has become a key factor impacting women's fertility.This article summarizes the multiple pathogenic mechanisms and signaling pathways involved in the occurrence and development of DOR, among which the Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/AKT) signaling pathway plays a core role in the regulation of ovarian function. The article demonstrates that the PI3K/AKT pathway exerts a significant effect on the pathogenesis of DOR: it influences the occurrence and progression of DOR by regulating granulosa cell apoptosis, modulating ovarian inflammatory responses, and governing the autophagy and oxidative stress processes of granulosa cells and follicular cells.Furthermore, this article focuses on summarizing the close association between the PI3K/AKT pathway and the pathogenic mechanism of DOR, as well as reviewing the latest experimental studies on the treatment of DOR using traditional Chinese medicine (TCM) monomers and compound prescriptions via this pathway, thereby providing references for the further advancement of DOR treatment research.

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  • 收稿日期:2025-09-26
  • 最后修改日期:2025-12-25
  • 录用日期:2026-02-06
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