The m6A-autophagy axis in reproductive physiology and disease: from epigenetic regulation to therapeutic resistance

N6-methyladenosine (m6A) modification and autophagy are two conserved systems that shape RNA fate, organelle turnover, and stress adaptation. In reproductive tissues, their crosstalk is particularly relevant because germ cells and early embryos repeatedly enter short developmental windows in which transcription is limited but rapid proteome remodeling is required. Here, we review the m6A-autophagy axis as an integrated epitranscriptomic-metabolic network in reproductive physiology, reproductive disease, environmental toxicology, and therapy resistance. We define m6A as a context-dependent fast switch that adjusts autophagic flux by altering the stability or translation of autophagy-related transcripts, including ULK1/2 , ATG5/7 , LC3B , SIRT1 , and BNIP3 . We further discuss reciprocal feedback, including autophagic turnover of YTHDF proteins and the emerging LC3B -mediated maternal mRNA decay model, while distinguishing well-supported mechanisms from findings that still require independent validation. Across polycystic ovary syndrome, premature ovarian insufficiency, reproductive tumors, and pollutant-induced reproductive injury, this axis may provide biomarkers and intervention points, but most evidence remains preclinical and cell-type specific. We therefore emphasize evidence strength, mechanistic boundaries, and translational barriers to guide future work in reproductive epitranscriptomics.