AI Article Synopsis
- * Researchers discovered that miR-106a inhibits essential processes such as cell proliferation, autophagy, and angiogenesis in venous endothelial cells while promoting cell death (apoptosis).
- * ATG7 was identified as a target gene of miR-106a, with findings suggesting that regulating this interaction could offer new therapeutic strategies for treating MI.
Article Abstract
Background: Myocardial infarction (MI) is an acute condition in which the heart muscle dies due to the lack of blood supply. Previous research has suggested that autophagy and angiogenesis play vital roles in the prevention of heart failure after MI, and miR-106a is considered to be an important regulatory factor in MI. But the specific mechanism remains unknown. In this study, using cultured venous endothelial cells and a rat model of MI, we aimed to identify the potential target genes of miR-106a and discover the mechanisms of inhibiting autophagy and angiogenesis.
Methods: We first explored the biological functions of miR-106a on autophagy and angiogenesis on endothelial cells. Then we identified ATG7, which was the downstream target gene of miR-106a. The expression of miR-106a and ATG7 was investigated in the rat model of MI.
Results: We found that miR-106a inhibits the proliferation, cell cycle, autophagy and angiogenesis, but promoted the apoptosis of vein endothelial cells. Moreover, ATG7 was identified as the target of miR-106a, and ATG7 rescued the inhibition of autophagy and angiogenesis by miR-106a. The expression of miR-106a in the rat model of MI was decreased but the expression of ATG7 was increased in the infarction areas.
Conclusion: Our results indicate that miR-106a may inhibit autophagy and angiogenesis by targeting ATG7. This mechanism may be a potential therapeutic treatment for MI.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11369033 | PMC |
| http://dx.doi.org/10.1002/ame2.12418 | DOI Listing |
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