| First Author | Tan S | Year | 2019 |
| Journal | FASEB J | Volume | 33 |
| Issue | 2 | Pages | 2000-2016 |
| PubMed ID | 30216111 | Mgi Jnum | J:284839 |
| Mgi Id | MGI:6388164 | Doi | 10.1096/fj.201800828RR |
| Citation | Tan S, et al. (2019) beta-Arrestin1 enhances liver fibrosis through autophagy-mediated Snail signaling. FASEB J 33(2):2000-2016 |
| abstractText | GPCR mediator beta-arrestins (beta-arr1 and beta-arr2) regulate a variety of physiologic and pathologic processes, including hepatocellular carcinogenesis. However, the role of beta-arrestins in liver fibrosis remains unknown. beta-arr1, but not beta-arr2, was upregulated in liver fibrotic tissues in both humans and mice; moreover, autophagy was increased. beta-arr1 deficiency or autophagic inhibitor 3-methyladenine (3-MA) significantly blocked autophagy and downregulated liver fibrosis. Furthermore, beta-arr1 enhanced hepatocyte compensatory proliferation, and hepatic stellate cell growth with activation via autophagy resulted in liver fibrosis. In the fibrosis, beta-arr1 promoted nuclear translocation of Snail by downregulation of glycogen synthase kinase-3beta, and the nuclear translocation of Snail was abrogated either by beta-arr1 deficiency or by 3-MA. These results suggest that beta-arr1 promotes liver fibrosis via autophagy-mediated Snail signaling, and beta-arr1 may be a therapeutic target for liver fibrosis.-Tan, S., Lu, Y., Xu, M., Huang, X., Liu, H., Jiang, J., Wu, B. beta-Arrestin1 enhances liver fibrosis through autophagy-mediated Snail signaling. |
