LncRNA and mRNA m6A modification profile and functional network in sepsis-induced acute lung injury

N 6 -methyladenosine (m 6 A) modification is crucial in sepsis-related organ damage, but its profiles in sepsis-induced acute lung injury (ALI) remain unclear. In this study, we elucidated the landscape and network of m 6 A modification in a rat model of lipopolysaccharide (LPS)-induced ALI. Total m 6 A levels in lung tissues from control and LPS-treated rats were determined using liquid chromatography tandem mass spectrometry. Epitranscriptomic microarray identified differentially m 6 A-modified mRNAs and long non-coding RNAs (lncRNAs). Bioinformatic analyses were performed to explore the functional implications of these differentially methylated transcripts. Selected methylated lncRNAs were further validated using m 6 A single-base site quantitative PCR. Results indicated significantly reduced total m 6 A levels in lung tissues from LPS-treated rats. 283 mRNAs showed decreased m 6 A modification levels and were enriched in immune response and inflammation pathways. Among the differentially expressed lncRNAs, LOC102551452 displayed m 6 A hypomethylation and negative correlation with neutrophil-related genes. These findings illuminate the potential role of m 6 A modification in immune and inflammation processes during sepsis-induced ALI, suggesting that targeting m 6 A modifications could be a potential therapeutic approach for sepsis-induced ALI.