Role of m6A modification in female infertility and reproductive system diseases

Jinyu Chen, Yiwei Fang, Ying Xu, Haotong Sun
International journal of biological sciences · 2022 · vol. 18(9) , pp. 3592–3604 · doi:10.7150/ijbs.69771 · PMID:35813486 · PMC9254474 · W4285017912
review OA: gold CC0 ⤵ 9 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

This review highlights how m6A modification and its associated proteins are involved in female infertility, reproductive system diseases, and reproductive tumors, presenting potential diagnostic and therapeutic targets.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

This paper is a narrative review examining how N6-methyladenosine (m6A) RNA modification and its regulatory “machinery” (writers METTL3/METTL14/WTAP/KIAA1429, erasers FTO/ALKBH5, and readers such as YTH domain proteins) contribute to female infertility and multiple reproductive system diseases. It describes evidence that m6A levels and specific regulators are altered in abnormal oogenesis and in conditions including reproductive system tumors, adenomyosis, endometriosis, premature ovarian failure, and PCOS, summarizing mechanisms such as effects on oocyte quality, mRNA stability, alternative splicing, nuclear export, and translation. The review explicitly notes that there is no single established treatment for several infertility-related disorders and emphasizes the need for further mechanistic targets, but it is limited by being a synthesis of published studies rather than new experiments. This paper is centrally about endometriosis and adenomyosis—specifically, it reviews how changes in m6A modification and its protein machineries are implicated in these diseases alongside other female reproductive disorders.

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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.

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Condition tags

endometriosisadenomyosisinfertility

MeSH descriptors

Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Infertility, Female Neoplasms Neoplasms Neoplasms Neoplasms Neoplasms

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (9)

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License: CC0 · commercial use OK