Abstract
Both fibrosis and cirrhosis of the liver are the end results of most kinds of chronic liver damage and represent a common but difficult clinical challenge throughout the world. The inhibition of the fibrogenic, proliferative, and migratory effects of hepatic stellate cells (HSCs) has become an experimental therapy for preventing and even reversing hepatic fibrosis. Furthermore, a complete understanding of the function of non-coding RNA-mediated epigenetic mechanisms in HSC activation may improve our perception of liver fibrosis pathogenesis. This review focuses on the evolving view of the molecular mechanisms by which HSC activation by miR-29a signaling may moderate the profibrogenic phenotype of these cells, thus supporting the use of miR-29a agonists as a potential therapy for treating liver fibrosis in the future.