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Abstract:
Activation of hepatic stellate cells (HSCs) plays a pivotal role in the development of liver fibrosis. C1q/tumor necrosis factor-related protein 3 (CTRP3), a member of CTRPs, was involved in fibrosis. However, little is known about the role of CTRP3 in liver fibrosis. This study aimed to determine its role in liver fibrosis and explore the possible mechanism. Our results demonstrated that CTRP3 was lowly expressed in liver fibrosis tissues and activated HSCs. Overexpression of CTRP3 inhibited the proliferation and migration of HSCs, as well as suppressed the expression of extracellular matrix (ECM) in transforming growth factor-beta 1 (TGF-beta 1)-stimulated HSC-T6 cells. Furthermore, CTRP3 overexpression greatly inhibited the expression level of phosphorylation of Smad3 in TGF-beta 1-stimulated HSC-T6 cells. In conclusion, the present study demonstrated that CTRP3 inhibited the proliferation and migration of TGF-beta 1-induced HSC-T6 cells and attenuated liver fibrosis, at least in part, through inhibiting the Smad signaling pathway. These findings suggest that CTRP3 may be a promising therapeutic target for the treatment of liver fibrosis. (C) 2017 Elsevier Masson SAS. All rights reserved.
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BIOMEDICINE & PHARMACOTHERAPY
ISSN: 0753-3322
Year: 2017
Volume: 89
Page: 1387-1391
3 . 4 5 7
JCR@2017
6 . 5 2 9
JCR@2020
ESI Discipline: PHARMACOLOGY & TOXICOLOGY;
ESI HC Threshold:118
JCR Journal Grade:2
CAS Journal Grade:3
Cited Count:
WoS CC Cited Count: 8
SCOPUS Cited Count: 10
ESI Highly Cited Papers on the List: 0 Unfold All
WanFang Cited Count:
Chinese Cited Count:
30 Days PV: 6