| Expression pattern: |
UP |
| Associated gene: |
ATG5, NOTCH1 |
| Associated microRNA: |
MIR30D |
| Biological function: |
circHECW2 promotes endothelial-mesenchymal transition and contributes to BBB/cerebrovascular damage; knockdown of circHECW2 inhibits Meth- or LPS-induced EndoMT in vitro and LPS-induced EndoMT in vivo. |
| Molecular mechanism: |
circHECW2 functions as an endogenous MIR30D sponge, suppressing MIR30D activity and increasing downstream ATG5 expression; the circHECW2-MIR30D-ATG5 axis regulates NOTCH1 signaling and the nonautophagic role of ATG5 in EndoMT. |
| Biological pathway or process: |
ceRNA regulation (promotes); Notch (promotes); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
Back-Splice Junction PCR / divergent primers PCR; RT-qPCR; FISH / smFISH; RNA Pull-Down; Transfection; Western Blot; IF (Immunofluorescence); In Vivo Animal Model; Bioinformatics Analysis |
| Clinical significance: |
Specific blockade of circHECW2 may be a potential therapeutic target for BBB damage, but no patient diagnostic or prognostic association was reported. |
| Description: |
circHECW2/circHecw2 is upregulated in Meth- or LPS-stimulated HBMECs and in the hippocampus of LPS-treated mice. It acts as an endogenous sponge for MIR30D, thereby increasing ATG5 and activating downstream NOTCH1 signaling to promote endothelial-mesenchymal transition and BBB/cerebrovascular damage. Knockdown of circHECW2 suppresses EndoMT in vitro and in vivo, suggesting potential therapeutic relevance for BBB integrity damage in drug abuse and neuroinflammatory contexts. |
| Confidence score: |
0.6683 |