Early growth response factor 3 may regulate coronary atherosclerosis through the NF-κB signaling pathway and VEGF

Zumureti Abudukeyimu1, Junyi Luo2, Fang Liu1

  • 1Department of General Practice, the Fifth Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, 830001, China.

Insights

Early Growth Response 3 (Egr3) gene expression is elevated in coronary artery disease (CAD) and promotes atherosclerosis by increasing inflammatory factors and lipid accumulation. Inhibiting Egr3 reduces these effects, suggesting Egr3 as a potential therapeutic target for CAD.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Inflammation Research

Background:

  • Coronary artery disease (CAD) is a complex condition involving inflammation and endothelial dysfunction.
  • The role of specific gene expression, such as Early Growth Response 3 (Egr3), in CAD pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the expression of Egr3, inflammatory cytokines (IL-1β, IL-6), vascular endothelial growth factor (VEGF), and NF-κB in CAD patients.
  • To explore the relationship between Egr3 gene expression and these molecules in the context of CAD.

Main Methods:

  • Recruited 132 CAD patients and 63 healthy controls.
  • Measured gene and protein expression using RT-qPCR, ELISA, and Western blotting.
  • Utilized an in vitro atherosclerosis model with human coronary artery endothelial cells (HCAECs) treated with ox-LDL.

Main Results:

  • Egr3 and IL-6 serum levels were higher in severe CAD patients compared to mild stenosis and controls.
  • Egr3 expression positively correlated with IL-6, IL-1β, and Gensini score.
  • Inhibition of Egr3 in vitro reduced inflammatory markers, lipid droplet formation, and lumen formation capacity.

Conclusions:

  • Egr3 gene expression plays a significant role in promoting atherosclerosis development.
  • Egr3 may induce inflammatory factors and affect lipid and lumen formation, contributing to CAD pathogenesis.
  • Egr3 represents a potential therapeutic target for managing atherosclerosis.
Abstract

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