The modulatory effect of triclosan on the reversion of the activated phenotype of LX-2 hepatic stellate cells.

Hepatic diseases leading to fibrosis affect millions of individuals worldwide and are a major public health challenge. Although, there have been many advances in understanding hepatic fibrogenesis, an effective therapy remains elusive. Studies focus primarily on activation of the hepatic stellate cells (HSCs), the principal fibrogenic cells in the liver; however, fewer numbers of studies have examined molecular mechanisms that deactivate HSC, controlling the profibrogenic phenotype.

MicroRNA-1254 contributes to the controlling of pro-fibrogenic environment in LX-2 cells by modulating SMAD3 and wound repair: new insights in hepatic fibrosis.

Hepatic fibrosis and its end-stage cirrhosis have increased worldwide, and, despite all the efforts, no successful therapy is available. More recently, the heptapeptide angiotensin-(1-7) [ang-(1-7)] was reported to be able to modulate liver fibrosis and even steatosis; however, the molecular bases of these effects are not clear. In this study, we investigated the overexpression of the microRNA-1254 in the human hepatic stellate cell line LX-2, based on the effect of the heptapeptide in such cells, previously, demonstrated by our research group.