, a novel long noncoding RNA regulating autophagy in the liver tissues of endotoxemic mice through a competing endogenous RNA mechanism.

Sepsis is an often-deadly complication of infection that can lead to multiple organ failure. Previous studies have demonstrated that autophagy has a protective effect on liver injury in sepsis. Here, we report a novel long noncoding RNA (lncRNA), named lipopolysaccharide (LPS)-induced liver autophagy regulator (), which was highly induced in the liver tissues of endotoxemic mice. deficiency significantly increased the susceptibility of mice to LPS. In contrast, overexpression rescued the liver injury mediated by deficiency and increased the survival of knockout mice with endotoxemia. Autophagy-related protein 13 (Atg13) is a potential downstream target gene of . deficiency notably decreased Atg13 expression and suppressed autophagy in the livers of mice challenged with LPS. A reporter gene assay showed that competitively adsorbed miR-705 to increase the expression of Atg13 in cultured cells, indicating that participates in the regulation of the autophagy in the liver tissues of endotoxemic mice through a competitive endogenous RNA mechanism. In summary, we identified a novel lncRNA, , as a hepatic autophagy regulator, which not only promotes our understanding of liver pathophysiology but also provides a potential therapeutic target and/or diagnostic biomarker for liver injury in endotoxemia.