TUG1 has been shown to be involved in diverse human diseases by regulating gene expression at transcriptional and post-transcriptional levels via interaction with miRNA or proteins. However, the role of TUG1 in liver fibrosis remains unclear. Here, we found that Tug1 is dysregulated in liver fibrosis according to the microarray analysis. Moreover, we investigated the expression files of Tugl by using CCl4- and BDL-induced liver fibrosis model mice as well as in the primary cells isolated from the mice. We demonstrated that Tug1 is over-expressed in the fibrotic livers and activated HSCs, but not injured hepatocytes. In addition, we assessed the function of Tug1 in HSCs and found that Tugl promotes the expression of alpha-SMA, Col1 alpha 1, Mmp2/9/10 and Timp1. Mechanically, Tug1 promotes the expression of these pro-fibrogenic genes by down-regulating miR-29b, thus accelerating the progression of liver fibrosis. Further study revealed that TUG1 was up-regulated in liver tissues of patients with cirrhosis. All together, our data indicate that TUGI might be a potential therapy target of liver fibrosis. (C) 2018 Elsevier Inc. All rights reserved.