Lipopolysaccharide-induced histone lactylation mediates m6A RNA modification causing mitochondrial dysfunction and pulmonary fibroblasts activation to exacerbate sepsis-associated pulmonary fibrosis.

This study established a mouse and cell model induced by lipopolysaccharides (LPS) to investigate the possible mechanisms of lactylation and METTL3-mediated m6A RNA modification in pulmonary fibroblast activation and sepsis-associated PF.

Measurement of cell number and viability in the study's cell samples was performed with Countstar Rigel S2 before single-cell analysis in the 2025 Respiratory research study.