التفاصيل البيبلوغرافية
| العنوان: |
MicroRNA-27b-3p down-regulates FGF1 and aggravates pathological cardiac remodelling. |
| المؤلفون: |
Li, Guoqi, Shao, Yihui, Guo, Hong Chang, Zhi, Ying, Qiao, Bokang, Ma, Ke, Du, Jie, Lai, Yong Qiang, Li, Yulin |
| المصدر: |
Cardiovascular Research; Jun2022, Vol. 118 Issue 9, p2139-2151, 13p |
| مصطلحات موضوعية: |
FIBROBLAST growth factors, CARDIAC hypertrophy, MICRORNA, ANGIOTENSIN II, HEART fibrosis |
| مستخلص: |
Aims The heart undergoes pathological remodelling under increased stress and neuronal imbalance. MicroRNAs (miRNAs) are involved in post-transcriptional regulation of genes in cardiac physiology and pathology. However, the mechanisms underlying miRNA-mediated regulation of pathological cardiac remodelling remain to be studied. This study aimed to explore the function of endogenous microRNA-27b-3p (miR-27b-3p) in pathological cardiac remodelling. Methods and results miR-27b-3p expression was elevated in the heart of a transverse aortic constriction (TAC)-induced cardiac hypertrophy mouse model. miR-27b-knockout mice showed significantly attenuated cardiac hypertrophy, fibrosis, and inflammation induced by two independent pathological cardiac hypertrophy models, TAC and Angiotensin II (Ang II) perfusion. Transcriptome sequencing analysis revealed that miR-27b deletion significantly down-regulated TAC-induced cardiac hypertrophy, fibrosis, and inflammatory genes. We identified fibroblast growth factor 1 (FGF1) as a miR-27b-3p target gene in the heart which was up-regulated in miR-27b-null mice. We found that both recombinant FGF1 (rFGF1) and inhibition of miR-27b-3p enhanced mitochondrial oxidative phosphorylation (OXPHOS) and inhibited cardiomyocyte hypertrophy. Importantly, rFGF1 administration inhibited cardiac hypertrophy and fibrosis in TAC- or Ang II-induced models and enhanced OXPHOS by activating PGC1α/β. Conclusions Our study demonstrated that miR-27b-3p induces pathological cardiac remodelling and suggests that inhibition of endogenous miR-27b-3p or administration of FGF1 might have the potential to suppress cardiac remodelling in a clinical setting. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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