| Expression pattern: |
UN |
| Associated gene: |
DNMT1/3a, Klotho, MPC1, MPC2 |
| Associated microRNA: |
miR-148b-3p |
| Biological function: |
Promotes glycolysis, mitochondrial dysfunction, cell senescence, lactate accumulation, and kidney injury in SAKI; circHIPK3 downregulation reduces glycolysis and improves mitochondrial function in SAKI mouse and cell models. |
| Molecular mechanism: |
circHIPK3 acts through the miR-148b-3p/DNMT1/3a/Klotho axis and reverses MPC1-mediated inhibition of lactate production, thereby increasing glycolysis and aggravating mitochondrial dysfunction and cell senescence. |
| Biological pathway or process: |
glycolysis (promotes); mitochondrial function (inhibits); other pathway/process (promotes); ceRNA regulation (other) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Transfection; CCK8; Western Blot; Flow Cytometry（Non-apoptosis/cycle）; In Vivo Animal Model; H&E Staining; ELISA |
| Clinical significance: |
These findings may provide novel insights into the application of circHIPK3 to the transitional medicine of SAKI. |
| Description: |
This study identifies circHIPK3 as a pathogenic regulator in septic acute kidney injury models. circHIPK3 promotes glycolysis, lactate production, mitochondrial dysfunction, and cell senescence through the miR-148b-3p/DNMT1/3a/Klotho axis and by counteracting MPC1-mediated inhibition of lactate production; silencing circHIPK3 improves mitochondrial function and kidney injury phenotypes. |
| Confidence score: |
0.4245 |