| Expression pattern: |
UP |
| Associated gene: |
Col1a1, Col3a1, AGO2, COL1A1, COL3A1 |
| Associated microRNA: |
miR-29b-3p |
| Biological function: |
circHIPK3 promotes myocardial fibrosis, cardiac fibroblast proliferation, cardiac hypertrophy and left ventricular dysfunction in diabetic cardiomyopathy; knockdown attenuates myocardial fibrosis and improves cardiac function. |
| Molecular mechanism: |
circHIPK3 acts as a competing endogenous RNA that suppresses miR-29b-3p and upregulates Col1a1 and Col3a1/COL1A1 and COL3A1, thereby increasing type I and III collagen synthesis and myocardial fibrosis. |
| Biological pathway or process: |
fibrosis (promotes); proliferation (promotes); ceRNA regulation (other); other pathway/process (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; IHC (Immunohistochemistry); IF (Immunofluorescence); H&E Staining; Western Blot; In Vivo Animal Model; Bioinformatics Analysis |
| Clinical significance: |
- |
| Description: |
In this mouse DCM study, circHIPK3 is upregulated in diabetic myocardium and in fibrotic cardiac fibroblast conditions. It promotes myocardial fibrosis and cardiac fibroblast proliferation through a ceRNA mechanism involving miR-29b-3p and Col1a1/Col3a1, leading to increased collagen I/III expression; circHIPK3 knockdown attenuates fibrosis and improves cardiac function. |
| Confidence score: |
0.8412 |