Long noncoding RNA myocardial infarction associated transcript promotes the development of thoracic aortic by targeting microRNA‐145 via the PI3K/Akt signaling pathway

2019 ◽  
Vol 120 (9) ◽  
pp. 14405-14413 ◽  
Author(s):  
Shiyuan Chen ◽  
Hu Chen ◽  
Chaowen Yu ◽  
Ran Lu ◽  
Tao Song ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Signaling Pathway ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Akt Signaling ◽  
Akt Signaling Pathway

A novel long noncoding RNA FAF inhibits apoptosis via upregulating FGF9 through PI3K/AKT signaling pathway in ischemia–hypoxia cardiomyocytes

2019 ◽  
Vol 234 (12) ◽  
pp. 21973-21987 ◽  
Author(s):  
Hao‐Jie Shi ◽  
Ming‐Wei Wang ◽  
Jia‐Teng Sun ◽  
Hao Wang ◽  
Ya‐Fei Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Akt Signaling ◽  
Akt Signaling Pathway

scholarly journals The mechanism of myocardial fibrosis is ameliorated by myocardial infarction-associated transcript through the PI3K/Akt signaling pathway to relieve heart failure

2021 ◽  
Vol 49 (7) ◽  
pp. 030006052110314
Author(s):  
Xingsheng Zhao ◽  
Yu Ren ◽  
Hongkun Ren ◽  
Yun Wu ◽  
Xi Liu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Signaling Pathway ◽  
Myocardial Fibrosis ◽  
Noncoding Rna ◽  
Akt Signaling ◽  
Inflammatory Factors ◽  
Akt Signaling Pathway

Objective This study aimed to investigate the role of long noncoding RNA (LncRNA) myocardial infarction-associated transcript (MIAT) in a heart failure (HF) model in vivo and in vitro by regulating the PI3K/Akt signaling pathway. Methods We established HF models in vivo and in vitro and evaluated the collagen content of these models and other factors. Results We found that when LncRNA MIAT was silenced, vascular endothelial growth factor, phosphorylated protein kinase B (Akt), and phosphorylated phosphoinositide 3-kinase (PI3K) mRNA and protein levels were significantly downregulated, which suggested that MIAT activated the PI3K/Akt signaling pathway. Akt and PI3K expression was not significantly changed. We also found that when LncRNA MIAT was silenced, collagen expression was significantly downregulated. This finding suggested that MIAT promoted myocardial fibrosis during the development of HF. The levels of inflammatory factors were also significantly reduced with silencing of LncRNA MIAT. This finding suggested that MIAT promoted the expression of inflammatory factors in myocardial fibrosis by activating the PI3K/Akt signaling pathway. Conclusion This study indicates that silencing LncRNA MIAT may improve myocardial fibrosis and alleviate HF through the PI3K/Akt signaling pathway, which may be helpful for patients with HF to obtain a better therapeutic effect.

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