| First Author | Chen B | Year | 2023 |
| Journal | Diab Vasc Dis Res | Volume | 20 |
| Issue | 3 | Pages | 14791641231172139 |
| PubMed ID | 37208852 | Mgi Jnum | J:338472 |
| Mgi Id | MGI:7510046 | Doi | 10.1177/14791641231172139 |
| Citation | Chen B, et al. (2023) miR-1187 induces podocyte injury and diabetic nephropathy through autophagy. Diab Vasc Dis Res 20(3):14791641231172139 |
| abstractText | MicroRNAs plays important roles in the progression of diabetic nephropathy (DN) and podocyte injury. This study aimed to investigate the role and regulation mechanism of miR-1187 during the development of DN and podocyte injury. The content of miR-1187 in podocytes was up-regulated under high glucose (HG) treatment and increased in kidney tissue of db/db mice (DN model mice) compared with control db/m mice. The administration of miR-1187 inhibitor could decrease podocyte apoptosis induced by HG and attenuate the decline in renal function and reduce proteinuria as well as glomerular apoptosis in db/db mice. Mechanistically, miR-1187 could inhibit the autophagy level in HG-exposed podocytes and glomerulus of DN mice. Moreover, miR-1187 inhibitor could reduce HG-stimulated podocyte injury and autophagy flux inhibition. The mechanism may depend on autophagy. In conclusion, targeting miR-1187 may be a new therapeutic target for improving the high glucose damage of podocytes and the progression of DN. |