| Expression pattern: |
UN |
| Associated gene: |
FTO, Col1a1, Col3a1, Acta2, Postn |
| Associated microRNA: |
- |
| Biological function: |
Cardiac inhibition of circ-ZNF609 attenuates DOX-induced cardiac dysfunction, cardiac injury, cardiac atrophy, cardiomyocyte apoptosis, and cardiac fibrosis without compromising the anti-tumor efficacy or DOX sensitivity in tumor-bearing female mice. |
| Molecular mechanism: |
circ-ZNF609 suppression may exert cardioprotective effects partly through FTO regulation, reducing cardiac RNA m6A methylation, and mitigating apoptosis and fibrosis in DOX-induced cardiotoxicity. |
| Biological pathway or process: |
apoptosis (promotes); fibrosis (promotes); m6A modification (promotes); drug resistance (other); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; In Vivo Animal Model; IF (Immunofluorescence); TUNEL |
| Clinical significance: |
Targeting cardiac circ-ZNF609 may serve as a promising therapeutic strategy for preventing DOX-induced cardiotoxicity without impairing the anti-tumor efficacy of DOX. |
| Description: |
This study investigates cardiac circ-ZNF609 inhibition in a DOX-treated, tumor-bearing female mouse model. Knockdown of circ-ZNF609 in the heart alleviates DOX-induced cardiotoxicity, including cardiac dysfunction, injury, atrophy, apoptosis, and fibrosis, while preserving DOX anti-tumor efficacy. The cardioprotective mechanism may involve increased FTO expression and reduced cardiac RNA m6A methylation. |
| Confidence score: |
0.3957 |