Liver fibrosis will be treated by a potential target
The outcome of hepatitis is either self recovery or its development into liver fibrosis or, further, liver cirrhosis. Liver fibrosis is the early pathological process of cirrhosis, which is considered a reversible, wound-healing response. Since no ideal drug is available for its therapy, liver fibrosis is currently considered to be a major worldwide health problem.
Previous studies have demonstrated that activin A is involved in hepatic fibrosis formation. However, the mechanism of the fibrotic process is not well understood. Activin receptor-interacting protein 2 (ARIP2) has been recently identified as a negative regulator of activin signal pathways. The fact that ARIP2 is highly expressed in the liver suggests that ARIP2 may participate in activin-induced anti-fibrosis in the liver.
A research article published on November 7 in the World Journal of Gastroenterology addresses this question. A research team led by Dr. ZH Liu from Jilin University spent more than five years researching ARIP2. The researchers used mouse Hepal-6 cells obtained from mouse a hepatoma cell line that had functions of hepatic parenchymal cells to investigate the effects of ARIP2 anti-fibrosis on the production of collagen type IV, which is a component of the extracellular matrix (ECM) in liver fibrosis.
One conclusion reported by the investigators is that the mode of expression regulation by various activators of signaling transduction, such as PMA, foskolin and LPS, has been characterized, and its negative effect on the production of collagen type IV revealed, using Hepal-6 cells.
An additional result was that the expression level of ARIP2 mRNA in the Hapel-6 cells was elevated 12 h after treatment with activin A and endotoxin LPS. Thus, it was concluded that ARIP2 participates in the negative feedback regulation of signal transduction in the late stage by affecting the expression of ActRIIA, which further suggests that ARIP2 might be a potential target for treatment of liver fibrosis induced by activin.