ArticleAnimal models and experimental medicine2024
MiR-106a targets ATG7 to inhibit autophagy and angiogenesis after myocardial infarction.
Article in Animal models and experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- LncRNAiScience · 2026Article
- Programmed Cell Death of Endothelial Cells in Ischemic Heart Disease: Mechanism and Potential Cell and Gene Therapeutic Prospects.Bioengineering (Basel, Switzerland) · 2026Review
- Gastric Juice miR-106a-5p as a Non-Invasive Biomarker of Neuroinflammation and Neurodegeneration: A Prospective Observational Study.Diseases (Basel, Switzerland) · 2026Article
- Bibliometric Analysis of Research on Traditional Chinese Medicine Treatment of Myocardial Infarction from 2007 to 2024 Based on the Web of Science Database.Current medicinal chemistry · 2026Article
- Harnessing miRNA therapeutics: a novel approach to combat heart and brain infarctions in atherosclerosis.Cell death discovery · 2025Review
- Advances in miRNA research: Unraveling the complexities of gene regulation.Animal models and experimental medicine · 2025Review
- Inhibition of miR-499a-5p Ameliorates Apoptotic and Autophagic Damage in Hypoxic Cardiomyocytes H9c2 Through Upregulation of ARGLU1.The Kaohsiung journal of medical sciences · 2025Article
- MiR-106a targets ATG7 to inhibit autophagy and angiogenesis after myocardial infarction.Animal models and experimental medicine · 2024Article
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14 authors.
Funding
Abstract
backgroundMyocardial 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.
methodsWe 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.
resultsWe 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.
conclusionOur 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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.