| Expression pattern: |
UP |
| Associated gene: |
AGO2, a-SMA, COL1A1, COL3A1 |
| Associated microRNA: |
miR-29b-3p |
| Biological function: |
Promotes cardiac fibroblast proliferation and migration, upregulates a-SMA, COL1A1 and COL3A1 expression, and promotes Ang II-induced cardiac fibrosis; circHIPK3 silencing attenuates cardiac fibrosis and improves diastolic function. |
| Molecular mechanism: |
circHIPK3 acts as a miR-29b-3p sponge in the cytoplasm and regulates miR-29b-3p target genes a-SMA, COL1A1 and COL3A1, thereby promoting cardiac fibroblast proliferation, migration and cardiac fibrosis. |
| Biological pathway or process: |
fibrosis (promotes); proliferation (promotes); migration (promotes); ceRNA regulation (promotes) |
| Detected method: |
Q
H
|
| Validation methods: |
Back-Splice Junction PCR / divergent primers PCR; RNase R Treatment; Sanger Sequencing; Actinomycin D / DRB Stability Assay; RT-qPCR; FISH / smFISH; Nuclear-Cytoplasmic Fractionation; RIP (RNA Immunoprecipitation); Luciferase Reporter Assay; Transfection; EdU Staining; Transwell Assay; IF (Immunofluorescence); Western Blot; IHC (Immunohistochemistry); In Vivo Animal Model; H&E Staining; Bioinformatics Analysis |
| Clinical significance: |
Potential new therapeutic target for the prevention or treatment of Ang II-induced cardiac fibrosis. |
| Description: |
In this study, mouse circHIPK3 is up-regulated in cardiac fibroblasts and heart tissues after Ang II treatment. circHIPK3 promotes cardiac fibroblast proliferation, migration and fibrotic marker expression by sponging miR-29b-3p and regulating COL1A1, COL3A1 and a-SMA; silencing circHIPK3 attenuates Ang II-induced cardiac fibrosis in vivo. |
| Confidence score: |
0.8415 |