Liver fibrosis is a persistent damage repair response triggered by various injury factors, which leads to an abnormal accumulation of extracellular matrix within liver tissue samples. The current clinical treatment of liver fibrosis is currently ineffective; therefore, elucidating the mechanism of liver fibrogenesis is of significant importance. Herein, the function and related mechanisms of lncRNA within hepatic fibrosis were investigated. expression was shown to be increased in mouse hepatic fibrotic tissue samples, and knockdown suppressed hepatic pathological injury and down-regulated the expression levels of fibrosis-associated proteins. Mechanistically, played a role in the early activation of mouse hepatic stellate cells (mHSCs) based on bioinformatics analysis, and was positively correlated with Igfbp3 expression. Further experimental results demonstrated that knockdown impeded mHSCs proliferation and activation and also downregulated the protein expression of Igfbp3. could interact with IGFBP3 and boost its protein stability, and overexpression of partially reversed the inhibition of mHSCsproliferation and activation by the knockdown of . In conclusion, LncRNA mediates liver fibrosis by targeting IGFBP3 and promoting its protein stability, thereby promoting mHSC proliferation and activation. has been identified as an underlying target for treating liver fibrosis.