Potential role of thymosin beta 4 in the treatment of nonalcoholic fatty liver disease.

Chronic diseases and translational medicine2017PMID: 29063072

View on PubMed DOI: 10.1016/j.cdtm.2017.06.003

Plain Language Summary

Review proposing thymosin β4 as a therapeutic candidate for NAFLD and its progression to NASH. Covers TB4's relevant mechanisms: reducing hepatic inflammation, protecting hepatocytes from apoptosis, inhibiting hepatic stellate cell activation, and reducing fibrosis through TGF-β and PI3K/AKT pathway modulation. Reviews preclinical evidence in fatty liver models and discusses TB4's potential to interrupt the NAFLD→NASH→cirrhosis progression—providing mechanistic rationale for TB4 in the most common chronic liver disease, affecting ~25% of the global population.

Abstract

As a result of increased prevalence of obesity worldwide, non-alcoholic fatty liver disease (NAFLD) has become one of the most common causes of chronic liver disease. Although most NAFLD cases remain benign, some progress to end-stage liver diseases such as cirrhosis and hepatocellular carcinoma. Therefore, treatment should be considered for NAFLD patients who are likely to progress to nonalcoholic steatohepatitis (NASH) or fibrosis. Thymosin beta 4 (Tβ4), a G-actin sequestering peptide, regulates actin polymerization in mammalian cells. In addition, studies have reported anti-inflammatory, insulin-sensitizing, and anti-fibrotic effects of Tβ4. However, no research has been done to investigate the effects of Tβ4 on NAFLD. Based on the findings above mentioned, we hypothesize that Tβ4 may represent an effective treatment for NAFLD.

Authors

Jiang, Yong; Han, Tao; Zhang, Zhi-Guang; Li, Man; Qi, Feng-Xiang; Zhang, Ying; Ji, Ying-Lan

Keywords

HypothesisNonalcoholic fatty liver diseaseNonalcoholic steatohepatitisThymosin beta 4