Transcriptomic Characterization of Lonrf1 at the Single-Cell Level Under Pathophysiological Conditions

The study explored the expression and role of Lonrf1 at the single-cell level under various pathophysiological conditions, including ageing, nonalcoholic steatohepatitis (NASH), and wound healing. Lonrf1 was ubiquitously expressed across tissues, with increased expression in liver sinusoidal endothelial cells (LSECs) and Kupffer cells with age, suggesting a role in ageing. In the liver, Lonrf1high LSECs activated NF-kB and p53 pathways while suppressing IFNa, IFNg, and proteasome signaling. During wound healing, Lonrf1high/p16low fibroblasts promoted cell growth, while Lonrf1high/p16high fibroblasts activated WNT signaling. The study found that Lonrf1 was not significantly involved in NASH pathogenesis but played a role in oxidative damage responses and tissue remodeling during wound healing. Further research using Lonrf1-deficient mice was recommended to clarify its role.