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miRNA-29 aggravates myocardial infarction via inhibiting the PI3K/mTOR/HIF1α/VEGF pathway
Xiaoxi Wang1, Yanning Liu2, Huiqing Hou3
1Department of Medical Examination Center, Hebei Medical University, Hebei General Hospital, Shijiazhuang 050051, Hebei, China.
Introduction:
MI is defined by the presence of myocardial necrosis, which is caused by acute and persistent ischemia and hypoxia of the coronary artery. In recent years, its incidence rate has been on the rise in China.
Methods:
GSE34198, GSE97320 and GSE141512 datasets were download for DEG analysis. KEGG pathway analysis, GO analysis, GSEA and PPI network construction were performed. Later, target genes of candidate miRNAs were predicted. Next, echocardiography was conducted to detect the effects of miR-29 on left ventricular structure and cardiac function in vivo, and H&E staining was adopted to study the effects of miR-29 on angiogenesis and fibrosis in vivo. Furthermore, Western blotting was employed to investigate the effects of miR-29 inhibition on the expressions of proteins related to the PI3K\mTOR\ HIF-1α\VEGF pathway.
Results:
There were 162 DEGs involved in MI. GO analysis revealed that inflammatory responses, negative regulation of apoptosis and innate immune response were the main enriched biological processes. KEGG analysis manifested that DEGs were mainly enriched in the PI3K/Akt signaling pathway, and GSEA demonstrated that they were mainly enriched in the PI3K/Akt/mTOR, HIF and VEGF pathways. Moreover, target gene prediction showed that miR-29 was lowly expressed in MI. According to Masson's trichrome staining, miR-29 inhibition promoted angiogenesis, reduced fibrosis, and increased the protein expressions of p-PI3K, p-mTOR, HIF-1α, and VEGF.
Conclusions:
MiR-29 may play an important role in the growth and development of MI. After inhibition of miR-29, the PI3K/mTOR/HIF-1α/VEGF pathway is activated to alleviate MI.
Insights
Myocardial infarction (MI) involves heart tissue death due to ischemia. Inhibiting miR-29 activates the PI3K/mTOR/HIF-1α/VEGF pathway, promoting recovery and reducing damage in myocardial infarction.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Myocardial infarction (MI) is characterized by myocardial necrosis from ischemia and hypoxia.
- The incidence of MI is increasing in China.
Purpose of the Study:
- To investigate the role of miR-29 in myocardial infarction.
- To explore the therapeutic potential of miR-29 inhibition in MI.
Main Methods:
- Differential gene expression (DEG) analysis using datasets GSE34198, GSE97320, and GSE141512.
- Bioinformatic analyses including KEGG pathway, Gene Ontology (GO), and Gene Set Enrichment Analysis (GSEA).
- In vivo studies using echocardiography, H&E staining, and Western blotting to assess miR-29's effects on cardiac function, angiogenesis, fibrosis, and key pathway proteins.
Main Results:
- 162 differentially expressed genes (DEGs) were identified in MI patients.
- GO analysis highlighted inflammatory responses and immune responses.
- KEGG and GSEA revealed enrichment in PI3K/Akt/mTOR, HIF, and VEGF pathways.
- miR-29 was found to be downregulated in MI.
- Inhibition of miR-29 promoted angiogenesis, reduced fibrosis, and increased p-PI3K, p-mTOR, HIF-1α, and VEGF protein levels.
Conclusions:
- miR-29 plays a significant role in the development of MI.
- Inhibition of miR-29 activates the PI3K/mTOR/HIF-1α/VEGF pathway, offering a potential therapeutic strategy to alleviate MI.
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