[1] Zhang Z, Zha Y, Hu W, et al. The autoregulatory feedback loop of microRNA-21/programmed cell death protein 4/activation protein-1 (MiR-21/PDCD4/AP-1) as a driving force for hepatic fibrosis development. J Biol Chem, 2013, 288: 37082-37093.
[2] Wu K, Ye C, Lin L, et al. Inhibiting miR-21 attenuates experimental hepatic fibrosis by suppressing both the ERK1 pathway in HSC and hepatocyte EMT. Clin Sci (Lond), 2016, 130: 1469-1480.
[3] Zhang J, Jiao J, Cermelli S, et al. miR-21 Inhibition Reduces Liver Fibrosis and Prevents Tumor Development by Inducing Apoptosis of CD24+ Progenitor Cells. Cancer Res, 2015, 75: 1859-1867.
[4] Rodrigues PM, Afonso MB, Simao AL, et al. miR-21 ablation and obeticholic acid ameliorate nonalcoholic steatohepatitis in mice. Cell Death Dis, 2017, 8: e2825.
[5] Kennedy LL, Meng F, Venter JK, et al. Knockout of microRNA-21 reduces biliary hyperplasia and liver fibrosis in cholestatic bile duct ligated mice. Lab Invest, 2016, 96: 1256-1267.
[6] Caviglia JM, Yan J, Jang MK, et al. MicroRNA-21 and Dicer are dispensable for hepatic stellate cell activation and the development of liver fibrosis. Hepatology, 2018, 67: 2414-2429.
[7] Xiao L, Feng Q, Liang S, et al. A catalog of the mouse gut metagenome. Nat Biotechnol, 2015, 33: 1103-1108.
[8] Acharya C, Sahingur SE, Bajaj JS. Microbiota, cirrhosis, and the emerging oral-gut-liver axis. JCI Insight, 2017, 2.
[9] Ebert MS, Sharp PA. Roles for microRNAs in conferring robustness to biological processes. Cell, 2012, 149: 515-524.
[10] Alberti C, Cochella L. A framework for understanding the roles of miRNAs in animal development. Development, 2017, 144: 2548-2559. |
