| Expression pattern: |
UP |
| Associated gene: |
CCAR2 |
| Associated microRNA: |
- |
| Biological function: |
circMETTL9 promotes oxidative stress, mitochondrial damage, and neuronal apoptosis; circMETTL9 knockdown reduces ROS production, reduces apoptosis, preserves mitochondrial function, and improves cell viability under oxidative stress. |
| Molecular mechanism: |
circMETTL9 binds to and positively regulates CCAR2, inducing oxidative stress and apoptosis through mitochondria-mediated Bax/Bcl-2/caspase-3 signaling. |
| Biological pathway or process: |
apoptosis (promotes); mitochondrial function (inhibits); other pathway/process (promotes) |
| Detected method: |
Q
H
|
| Validation methods: |
RT-qPCR; FISH / smFISH; IF (Immunofluorescence); RIP (RNA Immunoprecipitation); RNA Pull-Down; Transfection; CCK8; Annexin V/PI Flow Cytometry; Western Blot; In Vivo Animal Model; Bioinformatics Analysis |
| Clinical significance: |
CircMETTL9 may be a therapeutic target for mitigating neurological dysfunction, oxidative stress, and neuronal damage following TBI. |
| Description: |
This study identifies circMETTL9 as an up-regulated circRNA in TBI-related brain injury and H₂O₂-induced neuronal oxidative stress models. circMETTL9 promotes ROS production, mitochondrial dysfunction, and neuronal apoptosis by binding to and positively regulating CCAR2, engaging the mitochondria-mediated Bax/Bcl-2/caspase-3 apoptotic pathway. Silencing circMETTL9 is presented as a potential strategy to reduce secondary neuronal injury after TBI. |
| Confidence score: |
0.6585 |