Potential Role of Thymosin Beta 4 in Liver Fibrosis #MMPMID26006229
Kim J; Jung Y
Int J Mol Sci 2015[May]; 16 (5): 10624-35 PMID26006229show ga
Liver fibrosis, the main characteristic of chronic liver diseases, is strongly associated with the activation of hepatic stellate cells (HSCs), which are responsible for extracellular matrix production. As such, investigating the effective regulators controlling HSC activation provides important clues for developing therapeutics to inhibit liver fibrosis. Thymosin beta 4 (T?4), a major actin-sequestering protein, is known to be involved in various cellular responses. A growing body of evidence suggests that T?4 has a potential role in the pathogenesis of liver fibrosis and that it is especially associated with the activation of HSCs. However, it remains unclear whether T?4 promotes or suppresses the activation of HSCs. Herein, we review the potential role of T?4 in liver fibrosis by describing the effects of exogenous and endogenous T?4, and we discuss the possible signaling pathway regulated by T?4. Exogenous T?4 reduces liver fibrosis by inhibiting the proliferation and migration of HSCs. T?4 is expressed endogenously in the activated HSCs, but this endogenous T?4 displays opposite effects in HSC activation, either as an activator or an inhibitor. Although the role of T?4 has not been established, it is apparent that T?4 influences HSC activation, suggesting that T?4 is a potential therapeutic target for treating liver diseases.
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Int+J+Mol+Sci 2015 ; 16 (5): 10624-35
