The role of macrophages in METTL1-mediated m7G reacute inflammation

Our study demonstrated that METTL1 expression is significantly induced in macrophages in response to inflammatory stimuli. Furthermore, METTL1 promotes the differentiation of macrophages into a pro-inflammatory phenotype by enhancing the stability of internal SARM1 mRNA, which accelerates NAD decline and induces metabolic reprogramming in macrophages. Our work elucidates the poorly understood molecular mechanism by which m7G contributes to macrophage phenotype switching and acute inflammation, suggesting that targeting METTL1 may serve as a potential strategy for mitigating acute inflammation.