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

Guofeng Bai1,2,3, Jinghao Yang1,2, Weili Liao1,2

  • 1Guangdong Provincial Key Laboratory of Laboratory Animals, Guangdong Laboratory Animals Monitoring Institute, Guangzhou, China.

Animal Models and Experimental Medicine
|May 29, 2024
PubMed
Abstract

Insights

MicroRNA-106a (miR-106a) inhibits autophagy and angiogenesis after myocardial infarction (MI) by targeting ATG7. This finding reveals a potential therapeutic strategy for treating heart attack complications.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Signaling

Background:

  • Myocardial infarction (MI) leads to heart muscle death due to reduced blood supply.
  • Autophagy and angiogenesis are crucial for preventing heart failure post-MI.
  • miR-106a is implicated in MI, but its precise mechanism is unclear.

Purpose of the Study:

  • To identify miR-106a target genes.
  • To elucidate the mechanisms by which miR-106a affects autophagy and angiogenesis.
  • To investigate the role of miR-106a in a rat model of MI.

Main Methods:

  • Examined miR-106a's effects on endothelial cell proliferation, cell cycle, autophagy, and angiogenesis.
  • Identified ATG7 as a direct downstream target of miR-106a.
  • Assessed miR-106a and ATG7 expression in a rat MI model.

Main Results:

  • miR-106a inhibited endothelial cell proliferation, cell cycle, autophagy, and angiogenesis, while promoting apoptosis.
  • ATG7 was confirmed as a miR-106a target, and its restoration reversed miR-106a's inhibitory effects.
  • In MI hearts, miR-106a levels decreased, whereas ATG7 levels increased in infarction areas.

Conclusions:

  • miR-106a inhibits autophagy and angiogenesis by targeting ATG7.
  • This miR-106a/ATG7 pathway represents a potential therapeutic target for myocardial infarction.
Keywords:
ATG7miR‐106aangiogenesisautophagymiRNAsmyocardial infarction

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