| Expression pattern: |
UP |
| Associated gene: |
ATM, p53, BCL-2 |
| Associated microRNA: |
miR-567, miR-4677 5p, miR-4778 5p |
| Biological function: |
Contributes to an adaptive oxidative-stress response in AoSMCs, protects against oxidative stress-induced apoptosis and supports stress-resistant SMC phenotype in AAA. |
| Molecular mechanism: |
Regulation at ATM locus affecting ATM mRNA and ATM pathway activity (p53 phosphorylation), influencing apoptosis/survival; proposed miRNA-sponging model (binding sites predicted) but not fully validated in AoSMCs. |
| Biological pathway or process: |
apoptosis (inhibits); other pathway/process (other) |
| Detected method: |
Q
H
M
|
| Validation methods: |
Microarray; RNase R Treatment; divergent primers PCR; Sanger Sequencing; RT-qPCR; ISH (In Situ Hybridization); Nuclear-Cytoplasmic Fractionation; Digital PCR; Transfection; Western Blot; In Vivo Animal Model; CCK8 |
| Clinical significance: |
Circulating cATM was significantly higher in AAA patients, supporting its potential use as an AAA diagnostic biomarker; trend toward higher levels in ruptured AAA suggests possible negative prognostic indicator. |
| Description: |
cATM (hsa_circ_0003641), derived from the ATM locus, is up-regulated in AAA aortic tissue, AAA-derived smooth muscle cells, and patient serum. Functionally, higher cATM is associated with reduced vulnerability to oxidative stress and reduced apoptosis in AAA-derived AoSMCs, while cATM knockdown increases apoptosis and alters ATM mRNA regulation, supporting its role as an adaptive stress-response signature and potential circulating biomarker for AAA. |
| Confidence score: |
0.6816 |