Therefore, the purpose of this study is to investigate the miR-29a regulation of BRD4 signaling in a bile duct-ligation (BDL) animal model with regard to developing cholestatic liver fibrosis.
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.
This study was conducted to clarify the mechanism of anti-fibrotic effect of miR-29a and to explore if miR-29a is a promising candidate for nucleic acid medicine against liver fibrosis.
The down-regulation of miR-29a and miR-29b in male mouse livers correlated with the early development of liver fibrosis, as indicated by increased expressions of fibrotic markers in male mice relative to female mice.