| Expression pattern: |
UP |
| Associated gene: |
ADAM10, Ago2 |
| Associated microRNA: |
miR-143-3p |
| Biological function: |
Knockdown of circ-FNDC3B alleviated Ang-II-induced VSMC injury by improving viability and proliferation and reducing apoptosis, inflammation, and oxidative stress. |
| Molecular mechanism: |
circ-FNDC3B acts as a competing endogenous RNA for miR-143-3p to regulate ADAM10 expression. |
| Biological pathway or process: |
ceRNA regulation (promotes); apoptosis (promotes); proliferation (inhibits); inflammation (promotes); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RNase R Treatment; RT-qPCR; Clinical Sample Validation; Nuclear-Cytoplasmic Fractionation; Bioinformatics Analysis; Luciferase Reporter Assay; RIP (RNA Immunoprecipitation); Transfection; CCK8; EdU Staining; Annexin V/PI Flow Cytometry; ELISA; Western Blot |
| Clinical significance: |
circ-FNDC3B expression was positively correlated with the diameter of AAA in patients. |
| Description: |
This study identifies human circ-FNDC3B (hsa_circ_0006156) as an up-regulated circRNA in AAA aorta tissues and Ang-II-treated VSMCs. circ-FNDC3B promotes Ang-II-induced VSMC injury by acting as a ceRNA for miR-143-3p, thereby increasing ADAM10 expression and enhancing apoptosis, inflammation, oxidative stress, and impaired VSMC growth. Its expression also correlates positively with AAA diameter, suggesting potential relevance to AAA development. |
| Confidence score: |
0.7795 |