| Expression pattern: |
UP |
| Associated gene: |
PARP1, HMGB1 |
| Associated microRNA: |
miR-17-5p |
| Biological function: |
Aggravates oxidative mtDNA damage, mitochondrial dysfunction and cardiomyocyte apoptosis in septic cardiomyopathy. |
| Molecular mechanism: |
Acts as a miRNA sponge for miR-17-5p to enhance PARP1 expression, activating the PARP1/HMGB1 axis and promoting oxidative mtDNA damage. |
| Biological pathway or process: |
apoptosis (promotes); mitochondrial function (inhibits); oxidative phosphorylation (inhibits); other pathway/process (promotes); ceRNA regulation (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Transfection; CCK8; TUNEL; Annexin V/PI Flow Cytometry; Luciferase Reporter Assay; RIP (RNA Immunoprecipitation); Co-IP; Western Blot; ELISA; IF (Immunofluorescence); In Vivo Animal Model |
| Clinical significance: |
- |
| Description: |
CircTLK1 is up-regulated in LPS-stimulated human cardiomyocytes and in septic rat myocardium. It promotes cardiomyocyte apoptosis by sponging miR-17-5p to increase PARP1, thereby activating the PARP1/HMGB1 axis and aggravating oxidative mtDNA damage and mitochondrial dysfunction. |
| Confidence score: |
0.6331 |