FIGURE 6.

A proposed work model for LILAR regulating autophagy in the liver tissues of endotoxemic mice. Upon challenge with lipopolysaccharide (LPS), the expression level of a novel long noncoding RNA, LILAR, was increased in the liver tissues of mice. LILAR functions as a competing endogenous RNA (ceRNA) that sponges miR‐705 to upregulate the expression of autophagy‐related protein 13 (Atg13) by removing the suppressive miR‐705 bound to its 3′‐untranslated region (UTR). Increased expression of the Atg13 protein promotes the formation of the ULK1 (unc‐51‐like kinase 1) complex comprising FIP200, ATG13, and ATG101, which is necessary for phagophore formation and autophagy activity, resulting in a reduction in liver injury in mice subjected to LPS injection. LILAR deficiency downregulates Atg13 through a ceRNA mechanism and suppresses the autophagy activity of liver tissues induced by LPS, leading to an increased death rate in mice. The schematic was drawn with the help of Microsoft PowerPoint.