In light of the significant roles of LXRα in cholesterol and lipid metabolism, inflammation, apoptosis, autophagy, and cellular bioenergetics (PPARγ) (Jalil et al., 2019; Ricote et al., 2004; Graham and Allen, 2015; Yang et al., 2020; Chen et al., 2024b; Dixon et al., 2021) as well as the bioinformatics-based finding that LXRα is significantly downregulated in the sepsis-related lung injury mouse model, we mainly focused on the regulatory effects of LXRα on the inflammatory responses in sepsis-induced ALI. Here, NR1H3 is linked to acute respiratory distress syndrome.