The role of FSH and TGF-β superfamily in follicle atresia

Yu-Lan Chu¹, Ya-Ru Xu¹, Wan-Xi Yang¹, Yi Sun¹

¹College of Life Sciences, Zhejiang University, Hangzhou 310058, China

* * Equal contribution

Received: December 23, 2017Accepted: February 23, 2018Published: March 2, 2018

Copyright: © 2018 Chu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Most of the mammalian follicles undergo a degenerative process called “follicle atresia”. Apoptosis of granulosa cells is the main characteristic of follicle atresia. Follicle stimulating hormone (FSH) and the transforming growth factor β (TGF-β) superfamily have important regulatory functions in this process. FSH activates protein kinase A and cooperating with insulin receptor substrates, it promotes the PI3K/Akt pathway which weakens apoptosis. Both Smad or non-Smad signaling of the transforming growth factor β superfamily seem to be related to follicle atresia, and the effect of several important family members on follicle atresia is concluded in this article. FSH and TGF-β are likely to mutually influence each other and what we have already known about the possible underlying molecular mechanism is also discussed below.