| First Author | Yang S | Year | 2023 |
| Journal | iScience | Volume | 26 |
| Issue | 11 | Pages | 108131 |
| PubMed ID | 37867958 | Mgi Jnum | J:342076 |
| Mgi Id | MGI:7544661 | Doi | 10.1016/j.isci.2023.108131 |
| Citation | Yang S, et al. (2023) MircroRNA-92b as a negative regulator of the TGF-beta signaling by targeting the type I receptor. iScience 26(11):108131 |
| abstractText | Transforming growth factor beta1 (TGFbeta1) has been identified as a major pathogenic factor underlying the development of chronic kidney disease (CKD). This study investigated the role of miR-92b-3p in the progression of renal fibrosis in unilateral ureteral occlusion (UUO) and unilateral ischemia-reperfusion injury (uIRI) mouse models, as well as explored its underlying mechanisms in human proximal tubular epithelial (HK2) cells. We found that renal fibrosis increased in UUO mice after miR-92b knockout, while it reduced in miR-92b overexpressing mice. MiR-92b knockout aggravated renal fibrosis in uIRI mice. RNA-sequencing analysis, the luciferase reporter assay, qPCR analysis, and western blotting confirmed that miR-92b-3p directly targeted TGF-beta receptor 1, thereby ameliorating renal fibrosis by suppressing the TGF-beta signaling pathway. Furthermore, we found that TGF-beta suppressed miR-92b transcription through Snail family transcriptional repressors 1 and 2. Our results suggest that miR-92b-3p may serve as a novel therapeutic for mitigating fibrosis in CKD. |
