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Updated: Sep 30, 2025

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
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miRNA-29a inhibits atherosclerotic plaque formation by mediating macrophage autophagy via PI3K/AKT/mTOR pathway

Weihua Shao1, Suxing Wang2, Xiaoxi Wang3

  • 1Second Department of Geriatrics, Hebei Medical University and Hebei General Hospital, Shijiazhuang 050051, Hebei, China.

Aging
|March 15, 2022
PubMed
Abstract

Insights

MicroRNA-29a (miR-29a) elevation boosts autophagy by inhibiting the PI3K/AKT/mTOR pathway, offering a new therapeutic strategy for atherosclerosis (AS). This study clarifies miR-29a

Area of Science:

  • Biomedical research
  • Molecular biology
  • Cardiovascular science

Background:

  • Atherosclerosis (AS) pathogenesis involves microRNA-29a (miR-29a).
  • The precise role of the miR-29a-targeted PI3K signaling pathway in AS remains incompletely understood.

Purpose of the Study:

  • To investigate the functional relationship between miR-29a, the PI3K signaling pathway, and atherosclerosis.
  • To explore the therapeutic potential of modulating miR-29a in AS.

Main Methods:

  • Bioinformatic analysis of gene expression profiles from public databases (GEO).
  • In vivo (ApoE-/- mice) and in vitro (RAW264.7 cells) models of AS treated with miR-29a modulators.
  • Histological staining (MOVAT), Transmission Electron Microscopy (TEM), Western blotting, and immunofluorescence staining to assess molecular and cellular changes.

Main Results:

  • miR-29a was found to target PIK3CA, a key component of the PI3K pathway.
  • Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses indicated autophagy as a significantly enriched pathway in AS.
  • miR-29a suppressed atherosclerotic plaque size and macrophage accumulation, promoting M2-like polarization and inhibiting M1-like polarization.
  • miR-29a downregulated PI3K, p-PI3K, p-AKT, and p-mTOR, while upregulating autophagy markers Beclin 1 and LC3II.

Conclusions:

  • Elevated miR-29a promotes autophagy by downregulating the PI3K/AKT/mTOR pathway during AS progression.
  • miR-29a represents a potential novel therapeutic target for atherosclerosis.
Keywords:
PI3K/AKT/mTORatherosclerosisatheroscleroticmacrophagemiR-29aplaque

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