Open AccessUrsodesoxycholic acid alleviates liver fibrosis via proregeneration by activation of the ID1‐WNT2/HGF signaling pathway
Author(s) -
Dong Xi,
Luo Yun,
Lu Shan,
Ma Han,
Zhang Wenchao,
Zhu Yue,
Sun Guibo,
Sun Xiaobo
Publication year - 2021
Publication title -
clinical and translational medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.125
H-Index - 1
ISSN - 2001-1326
DOI - 10.1002/ctm2.296
Subject(s) - liver regeneration , medicine , fibrosis , cirrhosis , cancer research , cholestasis , hepatocyte growth factor , liver injury , hepatocyte , regeneration (biology) , gene knockdown , liver fibrosis , chemistry , biology , apoptosis , microbiology and biotechnology , biochemistry , receptor , in vitro
Background The human liver possesses a remarkable capacity for self‐repair. However, liver fibrosis remains a serious medical concern, potentially progressing to end‐stage liver cirrhosis and even death. Liver fibrosis is characterized by excess accumulation of extracellular matrix in response to chronic injury. Liver regenerative ability, a strong indicator of liver health, is important in resisting fibrosis. In this study, we provide evidence that ursodesoxycholic acid (UDCA) can alleviate liver fibrosis by promoting liver regeneration via activation of the ID1‐WNT2/hepatocyte growth factor (HGF) pathway. Methods Bile duct ligation (BDL) and partial hepatectomy (PH) mouse models were used to verify the effects of UDCA on liver fibrosis, regeneration, and the ID1‐WNT2/HGF pathway. An Id1 knockdown mouse model was also used to assess the role of Id1 in UDCA alleviation of liver fibrosis. Results Our results demonstrate that UDCA can alleviate liver fibrosis in the BDL mice and promote liver regeneration via the ID1‐WNT2/HGF pathway in PH mice. In addition, Id1 knockdown abolished the protection afforded by UDCA in BDL mice. Conclusions We conclude that UDCA protects against liver fibrosis by proregeneration via activation of the ID1‐WNT2/HGF pathway.