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Deficiency of GATA3-Positive Macrophages Improves Cardiac Function Following Myocardial Infarction or Pressure

Mingjie Yang1, Lei Song1, Lai Wang1

  • 1Oppenheimer Atherosclerosis Research Center, Cedars Sinai Smidt Heart Institute, and Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, California.

Journal of the American College of Cardiology
|August 18, 2018
PubMed

Insights

GATA3-positive macrophages worsen cardiac function after heart attack or pressure overload. Removing GATA3 in these cells improves heart function by altering inflammatory and reparative macrophage populations.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Macrophage Biology

Background:

  • Macrophages are key players in cardiovascular disease pathogenesis due to their plasticity.
  • Understanding macrophage subtypes and their roles is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of GATA3-positive macrophages in cardiac function following myocardial infarction (MI) and pressure overload.
  • To determine how GATA3 deficiency in myeloid cells impacts cardiac remodeling and function.

Main Methods:

  • Generated myeloid-specific GATA3-deficient (mGATA3KO) mice and control littermates.
  • Induced myocardial infarction (MI) and pressure overload models.
  • Assessed cardiac function using echocardiography, flow cytometry, and molecular analyses.

Main Results:

  • GATA3-positive macrophages accumulated in the myocardium post-MI.
  • mGATA3KO mice showed improved cardiac function after MI and pressure overload compared to controls.
  • Absence of GATA3 shifted macrophage populations towards a proinflammatory phenotype (Ly6C high) and away from a reparative phenotype (Ly6C low).

Conclusions:

  • GATA3-positive macrophages negatively impact cardiac remodeling and function after ischemic injury or pressure overload.
  • Eliminating GATA3 in macrophages improves cardiac outcomes, suggesting a therapeutic target.
  • Targeting GATA3 expression pathways in macrophages may offer a novel strategy for treating cardiovascular diseases.
Abstract

Keywords:
cardiac hypertrophyinflammationmacrophagetranscription factor

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