NRF1-enhanced miR-4458 alleviates cardiac hypertrophy through releasing TTP-inhibited TFAM.

摘要: Growing evidence suggests the crucial role of microRNAs (miRNAs) in regulating basic cell functions, and therefore participating pathologic development diverse human diseases, including cardiac hypertrophy. Herein, we explained that miR-4458 was distinctly stimulated Ang II-stimulated hypertrophic H9c2 cells. Intriguingly, inhibition led to exacerbated phenotypes II-treated In addition, compensatory upregulation cells ascribed its transcriptional enhancement by NRF1, a transcription factor previously identified be activated early Moreover, discovered served as negative modulator hypertrophy prompting TFAM, well-recognized myocardial protective protein. TTP, RBP always leads degradation recognized mRNAs, predicted interact with both TFAM mRNA. Importantly, verified facilitated expression cardiomyocytes directly targeting TTP releasing TTP-destabilized On whole, these findings demonstrated NRF1-induced boosted via dampen exacerbation hypertrophy, which indicates promising biomarker for treatment.