Progress of targeting transforming growth factor-β1 small interfering RNA in liver fibrosis.
- Author:
Xuan ZHOU
1
;
Xue-feng YANG
1
Author Information
1. Department of Gastroenterology, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421002, China.
- Publication Type:Journal Article
- MeSH:
Liver Cirrhosis;
therapy;
RNA, Small Interfering;
genetics;
Transforming Growth Factor beta1;
genetics
- From:
Chinese Medical Sciences Journal
2014;29(4):231-235
- CountryChina
- Language:English
-
Abstract:
Liver fibrosis is a common pathological consequence of a variety of chronic stimuli, including viral, autoimmune, drug-induced, cholestatic and metabolic diseases. Fibrosis is driven by a dynamic process involving increased synthesis of matrix components and a failure of physiological mechanisms of matrix turnover. Activation of hepatic stellate cells (HSCs) remains a central event in fibrosis. HSCs are the main source of extracellular matrix (ECM). Transforming growth factor-beta (TGF-Β), which is the fibrogenic master cytokine, can induce the activation of HSCs to produce a large amount of ECM, and is capable of inducing apoptosis of liver cells. RNA interference (RNAi) is a novel gene disruption technology. Studies have shown that small interfering RNA (siRNA) targeting TGF-Β1 may inhibit the activation and proliferation of HSCs, suppress ECM synthesis and block liver fibrosis. TGF-Β1 siRNA-mediated gene silencing therapy provides a new avenue for liver fibrosis. This review summarizes recent progresses in research on HSCs, TGF-Β1 and TGF-Β1 siRNA in liver fibrosis.
