| Expression pattern: |
UP |
| Associated gene: |
HMGA1 |
| Associated microRNA: |
miR-671-5p |
| Biological function: |
CDR1as promotes H/R-induced cardiomyocyte injury by reducing cell viability, promoting apoptosis, oxidative stress and inflammation, and weakening the protective effect of sevoflurane. |
| Molecular mechanism: |
CDR1as acts as a ceRNA that sponges miR-671-5p, relieving miR-671-5p-mediated inhibition of HMGA1 and thereby increasing HMGA1 levels in H/R cardiomyocytes. |
| Biological pathway or process: |
ceRNA regulation (other); proliferation (inhibits); apoptosis (promotes); inflammation (promotes); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Transfection; CCK8; Annexin V/PI Flow Cytometry; ELISA; Nuclear-Cytoplasmic Fractionation; RNA Pull-Down; Luciferase Reporter Assay; Bioinformatics Analysis |
| Clinical significance: |
- |
| Description: |
In H/R cardiomyocytes modeling MI/RI, CDR1as is up-regulated and contributes to cardiomyocyte injury by reducing viability and promoting apoptosis, oxidative stress and inflammation. Sevoflurane suppresses CDR1as, thereby inhibiting the CDR1as/miR-671-5p/HMGA1 ceRNA axis and exerting cardioprotective effects. |
| Confidence score: |
0.6528 |