# LncRNA Snhg12/IGFBP3 axis is involved in liver fibrosis by promoting the proliferation and activation of mouse hepatic stellate cells

## TL;DR

This study shows that the lncRNA Snhg12 promotes liver fibrosis by boosting the activity of hepatic stellate cells through its interaction with IGFBP3.

## Contribution

The study identifies Snhg12 as a novel regulator of liver fibrosis by stabilizing IGFBP3 protein in hepatic stellate cells.

## Key findings

- Snhg12 knockdown reduces liver fibrosis and fibrosis-associated protein expression in mice.
- Snhg12 promotes mouse hepatic stellate cell proliferation and activation via stabilizing IGFBP3 protein.
- Overexpression of IGFBP3 partially reverses the effects of Snhg12 knockdown.

## Abstract

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 Snhg12 within hepatic fibrosis were investigated. Snhg12 expression was shown to be increased in mouse hepatic fibrotic tissue samples, and Snhg12 knockdown suppressed hepatic pathological injury and down‐regulated the expression levels of fibrosis‐associated proteins. Mechanistically, Snhg12 played a role in the early activation of mouse hepatic stellate cells (mHSCs) based on bioinformatics analysis, and Snhg12 was positively correlated with Igfbp3 expression. Further experimental results demonstrated that Snhg12 knockdown impeded mHSCs proliferation and activation and also downregulated the protein expression of Igfbp3. Snhg12 could interact with IGFBP3 and boost its protein stability, and overexpression of Igfbp3 partially reversed the inhibition of mHSCsproliferation and activation by the knockdown of Snhg12. In conclusion, LncRNA Snhg12 mediates liver fibrosis by targeting IGFBP3 and promoting its protein stability, thereby promoting mHSC proliferation and activation. Snhg12 has been identified as an underlying target for treating liver fibrosis.

“lnc Snhg12/IGFBP3 axis promote liver fibrosis by promoting HSC proliferation and activation”.