Academic Journal

MiR‐106a targets ATG7 to inhibit autophagy and angiogenesis after myocardial infarction

التفاصيل البيبلوغرافية
العنوان: MiR‐106a targets ATG7 to inhibit autophagy and angiogenesis after myocardial infarction
المؤلفون: Guofeng Bai, Jinghao Yang, Weili Liao, Xiaofeng Zhou, Yingting He, Nian Li, Liuhong Zhang, Yifei Wang, Xiaoli Dong, Hao Zhang, Jinchun Pan, Liangxue Lai, Xiaolong Yuan, Xilong Wang
المصدر: Animal Models and Experimental Medicine, Vol 7, Iss 4, Pp 408-418 (2024)
بيانات النشر: Wiley, 2024.
سنة النشر: 2024
المجموعة: LCC:Medicine (General)
مصطلحات موضوعية: angiogenesis, ATG7, autophagy, miR‐106a, miRNAs, myocardial infarction, Medicine (General), R5-920
الوصف: 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.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2576-2095
Relation: https://doaj.org/toc/2576-2095
DOI: 10.1002/ame2.12418
URL الوصول: https://doaj.org/article/d3992b10826f4956ab8434c3de809747
رقم الانضمام: edsdoj.3992b10826f4956ab8434c3de809747
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:25762095
DOI:10.1002/ame2.12418