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Calcium-Sensing Receptor on Neutrophil Promotes Myocardial Apoptosis and Fibrosis After Acute Myocardial Infarction

Ziqi Ren1, Kelaier Yang2, Meng Zhao3

  • 1Department of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China; Department of Hyperbaric Oxygen, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.

The Canadian Journal of Cardiology
|April 1, 2020
PubMed

Insights

The calcium-sensing receptor (CaSR) activates the NLRP3 inflammasome in neutrophils, worsening heart damage after acute myocardial infarction (AMI). Inhibiting CaSR may treat heart failure in AMI patients.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Cell Biology

Background:

  • Neutrophil infiltration exacerbates inflammation in acute myocardial infarction (AMI).
  • The role of the calcium-sensing receptor (CaSR) in neutrophil-mediated inflammation is not well understood.
  • Investigating CaSR's effect on the NLRP3 inflammasome in neutrophils is crucial for understanding AMI.

Purpose of the Study:

  • To evaluate CaSR's regulatory effects on the NLRP3 inflammasome in neutrophils.
  • To explore CaSR's role in AMI-related ventricular remodeling.
  • To identify potential therapeutic targets for AMI-induced heart failure.

Main Methods:

  • Detected CaSR, NLRP3 inflammasome, and IL-1β expression in neutrophils from AMI patients and rats using western blotting and immunofluorescence.
  • Assessed cardiomyocyte apoptosis and cardiac fibrosis.
  • Utilized CaSR agonists (Calindol) and antagonists (Calhex-231) to study inflammasome activation and downstream effects.

Main Results:

  • CaSR, NLRP3 inflammasome, and IL-1β were upregulated in neutrophils from AMI patients and rats.
  • CaSR activation enhanced NLRP3 inflammasome activation and IL-1β release, promoting cardiomyocyte apoptosis and fibrosis.
  • CaSR inhibition by Calhex-231 reduced inflammasome activation and protected against cardiac remodeling.

Conclusions:

  • CaSR activation of the NLRP3 inflammasome in neutrophils contributes to ventricular remodeling post-AMI.
  • CaSR inhibition presents a potential therapeutic strategy for heart failure following AMI.
Abstract

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