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. In the present study, we evaluated cellular and molecular actions of the chemical triclosan (TCS) in reverting activated HSCs to a quiesced phenotype. We demonstrated that the inhibition of the enzyme fatty acid synthase by TCS in activated HSCs promotes survival of the cells and triggers cellular and molecular changes that promote cellular phenotypic reversion, offering potentially new therapeutic directions.

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. In addition, this miRNA was chosen based on the identification of putative binding site of this small molecule in the mRNA sequences of different molecular connectors of the AKT/ PI3K pathway, which is modulated by the heptapeptide and connects to the control of several cellular mechanisms, including proliferation, survival, migration, and even liver fibrogenesis. The results revealed an innovative function of the miR‐1254 in controlling SMAD3 and pro‐fibrosing elements as well as the wound healing response in LX‐2, attenuating the scaring repair of the injured tissue. The combined findings provide useful information for future studies on the controlling of hepatic fibrogenesis.