[1] PubMed ID: | 39947523 |
Disease Name: | Cardiomegaly |
Tissue: | Blood |
Dysfunction Pattern: | Down-Regulation |
Validated Method: | RT-PCR//Western blot//High-throughput sequencing |
Description: | Our results demonstrated that modulating tRF-16-R29P4PE expression significantly reduced brain natriuretic peptide (BNP) and free fatty acid levels while enhancing ATP production, glucose levels, and mitochondrial membrane potential. These effects were accompanied by the downregulation of PACE4, hypoxia-inducible factor-1α (HIF-1α), glucose transporter-4 (GLUT-4), and medium-chain acyl-CoA dehydrogenase (MCAD), as well as the upregulation of peroxisome proliferator-activated receptor α (PPARα). Animal experiments revealed that tRF-16-R29P4PE minic improved cardiac function, reduced myocardial fibrosis, and mitigated metabolic disorders and mitochondrial damage. |
Comparision: | Disease VS Control |
Mechanism: | Furthermore, co-immunoprecipitation (Co-IP) and molecular docking assays confirmed a direct interaction between PACE4 and HIF-1α, and luciferase reporter assays identified PACE4 as a direct target of tRF-16-R29P4PE. By regulating the PACE4 and HIF-1α/PPARα signaling pathways, tRF-16-R29P4PE alleviates PCH, providing a promising molecular target for therapeutic intervention. |
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