Fatty acid binding protein 3 activates endothelial adhesion of circulating monocytes and impairs endothelial

Yen-Wen Wu1,2,3, Jaw-Wen Chen2,4,5,6,7, Hao-Yuan Tsai1

  • 1Division of Cardiology, Cardiovascular Medical Center, Far Eastern Memorial Hospital, New Taipei City, Taiwan.

PubMed

Insights

Elevated fatty acid binding protein 3 (FABP3) is linked to coronary artery disease (CAD) and impairs blood vessel formation. This suggests FABP3 may be a therapeutic target for atherosclerosis.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pathophysiology

Background:

  • Atherosclerotic cardiovascular diseases, including coronary artery disease (CAD), stem from vascular inflammation and endothelial dysfunction.
  • Elevated fatty acid binding protein 3 (FABP3) is associated with cardiovascular diseases, but its precise role is not fully understood.

Purpose of the Study:

  • To investigate the role of FABP3 in impaired angiogenesis.
  • To elucidate the mechanisms by which FABP3 contributes to the development of atherosclerosis in CAD.

Main Methods:

  • Clinical observational study of 1104 patients to analyze serum FABP3 and cardiovascular events.
  • In vitro studies using primary cultured mononuclear cells, endothelial progenitor cells, and human coronary artery endothelial cells.
  • In vivo studies in mice using matrigel plug neovascularization and aortic ring assays.

Main Results:

  • Circulating FABP3 levels were higher in patients with cardiovascular events and CAD.
  • FABP3 increased the expression of adhesion molecules in mononuclear cells and caused endothelial cell dysfunction via the ERK/p38/STAT1/VEGF pathway.
  • FABP3 impaired angiogenesis in vivo and endothelial cell function under oxLDL or TNF-α stimulation.

Conclusions:

  • FABP3 plays a significant role in the clinical and pathological aspects of atherosclerotic CAD.
  • FABP3's impact on endothelial dysfunction and impaired angiogenesis highlights its potential as a therapeutic target for CAD.
Abstract

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