# Role of m6A modification in female infertility and reproductive system diseases

## TL;DR

This paper reviews how m6A RNA modification influences female infertility and reproductive diseases, highlighting its potential as a diagnostic and therapeutic target.

## Contribution

The paper systematically reviews the role of m6A modification in various female reproductive disorders and identifies potential diagnostic and therapeutic targets.

## Key findings

- m6A modification is dynamically regulated by writers, erasers, and readers in reproductive processes.
- Abnormal m6A levels are linked to diseases like endometriosis and ovarian failure.
- m6A and its associated proteins show promise as biomarkers for reproductive dysfunction.

## Abstract

Gamete abnormalities and reproductive system tumors have become a dominant cause of infertility, troubling people globally. In recent years, increasing evidence emerged and found that N6-methyladenosine (m6A) played a leading role in reproduction. The biological effects of m6A modification are dynamically and reversibly regulated by methyltransferases (writers), WTAP, METTL3, METTL14 and KIAA1429, demethylases (erasers), FTO and ALKBH5, and m6A binding proteins (readers), including YTH domain. In this review, we highlight the change of m6A modification in abnormal oogenesis, female reproductive system diseases including reproductive system tumors, adenomyosis, endometriosis, premature ovarian failure and polycystic ovary syndrome. Moreover, we review some of the mechanisms and the specific modified genes that have been identified. Especially, with the underlying mechanisms being uncovered, m6A and its protein machineries are expected to be the markers and targets for the diagnosis and treatment of female reproductive dysfunction.