Findings show ALKBH5 drives inflammation and autophagy in LPS-stimulated macrophages, suggesting a new therapeutic target for ARDS.
Our findings demonstrate that ALKBH5-driven m⁶A demethylation of ULK1 exacerbates ARDS by promoting macrophage autophagy and pro-inflammatory responses. These results suggest that targeting ALKBH5 may disrupt pathogenic m6A demethylation, offering a novel therapeutic strategy for mitigating ARDS progression.
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Wang et al. (2026) studied this question.
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