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长链非编码RNA在人类卵巢储备功能下降致病机制中的作用

Role of lncRNAs in the pathogenic mechanism of human decreased ovarian reserve.

作者信息

Lv Zhexi, Lv Zekai, Song Linjiang, Zhang Qinxiu, Zhu Shaomi

机构信息

School of Medical and Life Sciences/Affiliated Reproductive and Women-Children Hospital, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.

State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.

出版信息

Front Genet. 2023 Feb 8;14:1056061. doi: 10.3389/fgene.2023.1056061. eCollection 2023.

DOI:10.3389/fgene.2023.1056061
PMID:36845376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9944763/
Abstract

Decreased ovarian reserve (DOR) is defined as a decrease in the quality and quantity of oocytes, which reduces ovarian endocrine function and female fertility. The impaired follicular development and accelerated follicle atresia lead to a decrease in the number of follicles, while the decline of oocyte quality is related to the disorder of DNA damage-repair, oxidative stress, and the dysfunction of mitochondria. Although the mechanism of DOR is still unclear, recent studies have found that long non-coding RNA (lncRNA) as a group of functional RNA molecules participate in the regulation of ovarian function, especially in the differentiation, proliferation and apoptosis of granulosa cells in the ovary. LncRNAs participate in the occurrence of DOR by affecting follicular development and atresia, the synthesis and secretion of ovarian hormones. This review summarizes current research on lncRNAs associated with DOR and reveals the potential underlying mechanisms. The present study suggests that lncRNAs could be considered as prognostic markers and treatment targets for DOR.

摘要

卵巢储备功能下降(DOR)被定义为卵母细胞的质量和数量减少,这会降低卵巢内分泌功能和女性生育能力。卵泡发育受损和卵泡闭锁加速导致卵泡数量减少,而卵母细胞质量下降与DNA损伤修复紊乱、氧化应激和线粒体功能障碍有关。尽管DOR的机制仍不清楚,但最近的研究发现,长链非编码RNA(lncRNA)作为一组功能性RNA分子参与卵巢功能的调节,特别是在卵巢颗粒细胞的分化、增殖和凋亡过程中。lncRNAs通过影响卵泡发育和闭锁、卵巢激素的合成和分泌参与DOR的发生。本综述总结了目前关于与DOR相关的lncRNAs的研究,并揭示了潜在的机制。本研究表明,lncRNAs可被视为DOR的预后标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1549/9944763/4db308e6f1c3/fgene-14-1056061-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1549/9944763/4db308e6f1c3/fgene-14-1056061-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1549/9944763/4db308e6f1c3/fgene-14-1056061-g001.jpg

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本文引用的文献

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Evaluation of FMR4, FMR5 and FMR6 Expression Levels as Non-Invasive Biomarkers for the Diagnosis of Fragile X-Associated Primary Ovarian Insufficiency (FXPOI).评估FMR4、FMR5和FMR6表达水平作为诊断脆性X相关原发性卵巢功能不全(FXPOI)的非侵入性生物标志物。
J Clin Med. 2022 Apr 14;11(8):2186. doi: 10.3390/jcm11082186.
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Translation regulatory long non-coding RNA 1 (TRERNA1) sponges microRNA-23a to suppress granulosa cell apoptosis in premature ovarian failure.翻译调节长非编码 RNA 1(TRERNA1)通过海绵吸附 microRNA-23a 抑制早发性卵巢功能衰竭中颗粒细胞凋亡。
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补肾活血方治疗卵巢储备功能下降:代谢组学与整合网络药理学联合分析
Heliyon. 2023 Sep 13;9(9):e20104. doi: 10.1016/j.heliyon.2023.e20104. eCollection 2023 Sep.
Transplantation of human umbilical cord mesenchymal stem cells to treat premature ovarian failure.
人脐带间充质干细胞移植治疗卵巢早衰。
Stem Cell Res Ther. 2021 Aug 11;12(1):454. doi: 10.1186/s13287-021-02529-w.
4
LncRNA ZNF674-AS1 regulates granulosa cell glycolysis and proliferation by interacting with ALDOA.长链非编码RNA ZNF674-AS1通过与醛缩酶A相互作用调控颗粒细胞糖酵解和增殖。
Cell Death Discov. 2021 May 16;7(1):107. doi: 10.1038/s41420-021-00493-1.
5
lncRNA promotes apoptosis of granulosa cells by targeting the miR-543-3p/DCN/TGF-β signaling pathway in Hu sheep.长链非编码RNA通过靶向湖羊中的miR-543-3p/核心蛋白聚糖/转化生长因子-β信号通路促进颗粒细胞凋亡。
Mol Ther Nucleic Acids. 2021 Mar 1;24:223-240. doi: 10.1016/j.omtn.2021.02.030. eCollection 2021 Jun 4.
6
lncRNA MALAT1 Regulates Mouse Granulosa Cell Apoptosis and 17-Estradiol Synthesis via Regulating miR-205/CREB1 Axis.长链非编码 RNA MALAT1 通过调控 miR-205/CREB1 轴调控小鼠颗粒细胞凋亡和 17β-雌二醇合成。
Biomed Res Int. 2021 Feb 17;2021:6671814. doi: 10.1155/2021/6671814. eCollection 2021.
7
Lnc-GULP1-2:1 affects granulosa cell proliferation by regulating COL3A1 expression and localization.Lnc-GULP1-2:1 通过调节 COL3A1 的表达和定位影响颗粒细胞的增殖。
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Hypermethylation-mediated downregulation of lncRNA PVT1 promotes granulosa cell apoptosis in premature ovarian insufficiency via interacting with Foxo3a.lncRNA PVT1 的高甲基化下调通过与 Foxo3a 相互作用促进早发性卵巢功能不全中的颗粒细胞凋亡。
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Overexpression of long non-coding RNA nuclear enriched abundant transcript 1 inhibits the expression of p53 and improves premature ovarian failure.长链非编码核糖核酸核富集丰富转录本1的过表达抑制p53的表达并改善卵巢早衰。
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