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Chemokine Fractalkine and Non-Obstructive Coronary Artery Disease-Is There a Link?

Aleksandra Stangret1, Karol Artur Sadowski2, Konrad Jabłoński2

  • 1Chair and Department of Experimental and Clinical Physiology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Banacha 1b, 02-097 Warsaw, Poland.

International Journal of Molecular Sciences
|April 13, 2024
PubMed

Insights

Non-obstructive coronary artery disease (NO-CAD) involves inflammation, with fractalkine (FKN/CX3CL1) playing a key role. Targeting FKN/CX3CL1 may offer new therapeutic avenues for NO-CAD patients.

Area of Science:

  • Cardiology
  • Immunology
  • Vascular Biology

Background:

  • Non-obstructive coronary artery disease (NO-CAD) is characterized by <50% coronary artery narrowing with a fractional flow reserve (FFR) ≤0.80.
  • Inflammation, atherosclerosis, and microvascular dysfunction are central to NO-CAD pathogenesis, though not fully understood.
  • Fractalkine (FKN/CX3CL1), an immune cell chemoattractant, is implicated in cardiovascular risk factors and inflammation.

Purpose of the Study:

  • To review current data on FKN/CX3CL1 in NO-CAD.
  • To explore the complex relationship between FKN/CX3CL1 and NO-CAD.
  • To present novel clinical implications of FKN/CX3CL1 in NO-CAD pathomechanism.

Main Methods:

  • Literature review of existing studies on FKN/CX3CL1 and NO-CAD.
  • Analysis of FKN/CX3CL1's role in immune cell function and vascular inflammation.
  • Evaluation of preliminary data on FKN/CX3CL1 inhibitors (e.g., KAND567) in related cardiovascular conditions.

Main Results:

  • FKN/CX3CL1 concentrations correlate positively with cardiovascular risk factors.
  • FKN/CX3CL1 promotes immune cell recruitment and survival, contributing to inflammation.
  • Preliminary studies show FKN/CX3CL1 inhibition (KAND567) reduces hyperinflammation in ST-elevation myocardial infarction (STEMI) patients.

Conclusions:

  • The link between FKN/CX3CL1 and NO-CAD is evident but requires further investigation.
  • FKN/CX3CL1's unique structure and function offer potential as a therapeutic target in NO-CAD.
  • Understanding FKN/CX3CL1's role may unveil novel clinical strategies for managing NO-CAD.

Keywords:
fractalkine/CX3CL1non-obstructive coronary artery disease

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