Transcriptomic characterization of Lonrf1 at the single-cell level under pathophysiological conditions

The study investigated the expression and function of Lonrf1 at the single-cell level under normal and pathological conditions. Lonrf1 was found to be ubiquitously expressed across various tissues, with increased expression in liver sinusoidal endothelial cells (LSECs) and Kupffer cells with age. In the liver, Lonrf1high LSECs activated NF-kB and p53 pathways while suppressing IFNa, IFNg, and proteasome signaling, independent of p16 expression. During wound healing, Lonrf1high/p16low fibroblasts promoted cell growth and suppressed TGFb and BMP signaling, whereas Lonrf1high/p16high fibroblasts activated WNT signaling. The findings suggested that LONRF1 played a crucial role in oxidative damage responses and tissue remodeling during wound healing, operating differently in senescent and nonsenescent cells.