HSC-specific knockdown of GGPPS alleviated CCl4-induced chronic liver fibrosis through mediating RhoA/Rock pathway.
Year: 2019
Type: article
Abstract: . Furthermore, our in vitro studies showed that GGPPS was up-regulated during HSCs activation in TGF-β1-dependent manner. Inhibition of GGPPS suppressed TGF-β1 induced F-actin reorganization and HSCs activation in LX-2 cells. Further, we found that GGPPS regulated HSCs activation and liver fibrosis possibly by enhancing RhoA/Rock kinase signaling. So its concluded that GGPPS promotes liver fibrosis by activating HSCs, which may represent a potential target for anti-fibrosis therapies.
Source: PubMed
Institutions: Nanjing Normal University, Nanjing University, Nanjing Drum Tower Hospital, Shanghai Jiao Tong University, Shanghai Chest Hospital, Model Animal Research Center, National Laboratory of Solid State Microstructures, China Pharmaceutical University, State Key Laboratory of Pharmaceutical Biotechnology, Nanjing Medical University
Language: English
Subfield: Hepatology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2981494272