SPOCK1: New Mechanistic Insight into Liver Fibrosis

Abstract

Chronic liver diseases with different etiologies can provoke a fibrotic wound-healing response, which leads to liver fibrosis. Liver fibrosis is characterized by abnormal deposition and distribution of extracellular matrix (ECM), which restricts the regeneration of normal liver, and finally results in liver cirrhosis, liver failure or even hepatocellular carcinoma (HCC) [1]. Etiologically, about 40% of HCC is caused by hepatitis B virus (HBV), 40% caused by hepatitis C virus (HCV), 11% caused by chronic alcohol abuse, and about 10% due to other causes, with an increasing prevalence of nonalcoholic fatty liver disease, and all these etiologies could lead to liver fibrosis, and contribute to a favorable niche for tumorgenesis [2]. Globally, liver cirrhosis currently accounts for approximately 1.16 million death each year, which ranks the 11th most common causes of death [2]. Despite increasing development of therapeutic strategies in the past two decades, there is still no approved anti-fibrotic drug to date [3]. Therefore, it is urgent to make further elucidation of the mechanism of liver fibrogenesis.