| Expression pattern: |
UP |
| Associated gene: |
tCDYL-100, METTL3, YTHDF3, REST, CDYL, EHMT2, rhoa, nppb, RhoA, BNP |
| Associated microRNA: |
- |
| Biological function: |
circCDYL promotes cardiomyocyte hypertrophy in vitro and aggravates Ang II-induced pathological cardiac hypertrophy in vivo; silencing circCDYL attenuates cardiac hypertrophy. |
| Molecular mechanism: |
circCDYL is N6-methylated and translated into tCDYL-100; tCDYL-100 competes with CDYL for REST binding, disrupts the REST-CDYL-EHMT2 transcription repression complex, retains REST in the cytoplasm, reduces promoter H3K9me2 repression, and activates prohypertrophic genes including rhoa and nppb. |
| Biological pathway or process: |
other pathway/process (promotes); m6A modification (other) |
| Detected method: |
Q
S
|
| Validation methods: |
Back-Splice Junction PCR / divergent primers PCR; RNase R Treatment; Sanger Sequencing; circRNA-seq; RT-qPCR; FISH / smFISH; IF (Immunofluorescence); RIP (RNA Immunoprecipitation); RNA Pull-Down; ChIP / ChIP-seq; Luciferase Reporter Assay; MeRIP / MeRIP-seq; Transfection; Western Blot; In Vivo Animal Model; H&E Staining; Bioinformatics Analysis |
| Clinical significance: |
- |
| Description: |
circCDYL is an Ang II-induced, conserved cardiac circRNA derived from cdyl/CDYL that promotes cardiomyocyte hypertrophy and worsens pathological cardiac hypertrophy. It functions by m6A-dependent translation of tCDYL-100, which antagonizes CDYL-mediated REST-EHMT2 transcriptional repression and activates prohypertrophic genes such as rhoa and nppb. Silencing circCDYL in mouse hearts attenuates Ang II-induced hypertrophy, suggesting a potential therapeutic target. |
| Confidence score: |
0.8165 |