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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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Autophagy-Related Genes in Atherosclerosis

Yuankun Chen1,2, Ao Zeng1, Shumiao He1,3

  • 1School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, China.

Journal of Healthcare Engineering
|July 26, 2021
PubMed

Insights

Autophagy-related genes (ARGs) are crucial in atherosclerosis (AS). This study analyzed differentially expressed ARGs, revealing their role in AS pathophysiology and potential for treating cardiovascular diseases (CVDs).

Area of Science:

  • Biomedical research
  • Molecular biology
  • Genetics

Background:

  • Atherosclerosis (AS) is a chronic inflammatory vascular disease and a primary cause of cardiovascular/cerebrovascular diseases (CVDs).
  • Autophagy-related genes (ARGs) are integral to AS pathophysiological processes.
  • The expression profiles of ARGs have been underexplored in the context of autophagy and AS.

Purpose of the Study:

  • To investigate the relationship between autophagy and AS by analyzing the expression profile of ARGs.
  • To identify potential therapeutic targets for CVDs by understanding the role of ARGs in AS.

Main Methods:

  • Utilized the GSE57691 dataset containing aortic atheroma and normal aortic tissues.
  • Analyzed differentially expressed ARGs using protein-protein interaction (PPI), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses.
  • Explored related microRNAs (miRNAs) and transcription factors through network analysis.

Main Results:

  • Identified 41 differentially expressed ARGs in the GSE57691 dataset.
  • GO and KEGG analyses indicated enrichment in autophagy, autophagosome, and related signaling pathways.
  • Highlighted key ARGs (ATG5, MAP1LC3B, MAPK3, MAPK8, RB1CC1) and identified 11 miRNAs and 6 transcription factors involved in regulatory networks.

Conclusions:

  • Autophagy and ARGs significantly influence the pathophysiology of AS.
  • Findings provide new insights into the molecular mechanisms of AS and potential therapeutic strategies for CVDs.
Abstract

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