# Decoding m6A: a new frontier in maternal-foetal immunology

## TL;DR

This review explores how m6A RNA modifications influence the maternal-foetal immune environment and their potential as biomarkers for pregnancy-related diseases.

## Contribution

The paper systematically outlines m6A's regulatory network during pregnancy and its role in maternal-foetal immunology.

## Key findings

- m6A modifications are dynamically regulated by writer, eraser, and reader proteins during pregnancy.
- m6A influences RNA metabolism and gene expression in maternal-foetal immune interactions.
- The study highlights gaps in understanding m6A's role in pregnancy disorders and its clinical potential.

## Abstract

m6A is the predominant internal RNA modification in eukaryotic cells and is distinguished by its abundance and evolutionary conservation. This epigenetic mechanism is dynamically controlled by a coordinated system of writer, eraser, and reader proteins. This sophisticated posttranscriptional regulatory mechanism precisely controls gene expression by influencing RNA metabolism, including its stability, translation, and splicing. Recent advances have revealed the functions of m6A in female reproductive cancers, early embryonic development, and stem cell differentiation. However, its functional roles and molecular mechanisms throughout pregnancy and in related disorders remain incompletely understood, which, to some extent, limits its clinical translation. This review systematically outlines the core regulators of m6A, advanced detection technologies, and its regulatory network across the continuum of pregnancy. Given the immunological parallels between the maternal–foetal interface and the tumour microenvironment, we discuss the possible function of m6A modifications in regulating the maternal–foetal immune microenvironment. The aims of this review were to elucidate the m6A regulatory network across gestation and evaluate its potential as a source of diagnostic biomarkers and therapeutic targets for pregnancy-related pathologies.