Letter to the Editor

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Dysregulation of follicle fatty acid is a potential driver of human primary ovarian insufficiency
Lina Wang1,2,3,† , Jihong Ma4,5,† , Yixin Kang6 , Na Zhang4,5 , Xinyu Li4,5 , Hao Wang4 , Donghong Song4 , Mo Li4,5,* , Huafang Gao2,* , Xiumei Zhen4,5,*
1Peking Union Medical College Graduate School, Beijing 100000, China
2National Research Institute for Health and Family Planning, Beijing 100000, China
3Reproductive Medicine Center of Henan Provincial People’s Hospital, Zhengzhou 450003, China
4Center for Reproductive Medicine, Peking University Third Hospital, Beijing 100191, China
5National Clinical Research Center for Obstetrics and Gynecology, Beijing 100191, China
6Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto M5S3M2, Canada
These authors contributed equally to this work.
*Correspondence to:Mo Li , Email:limo@hsc.pku.edu.cn Huafang Gao , Email:gaohuafang@nrifp.org.cn Xiumei Zhen , Email:xmzhen1970@aliyun.com
J Mol Cell Biol, Volume 12, Issue 10, October 2020, 817-819,  https://doi.org/10.1093/jmcb/mjaa044

Dear Editor,

Primary ovarian insufficiency (POI) is defined as a significant reduction of the follicle pool and induction of amenorrhea before the age of 40 (Nelson, 2009), associated with a decreased level of estrogen and hypergonadotropic state in the blood. Since POI patients have few follicles, it is difficult to obtain human oocytes to decipher this disease. In mammalian ovary, granulosa cells establish direct communication with oocytes and modulate transcription and chromatin remodeling of the oocyte (De La Fuente and Eppig, 2001). However, the whole-genomic DNA methylation profile of human granulosa cells and the potential clinical insights are absent.