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Endothelial CD36 mediates diet-induced increases in aortic stiffness.

Javad Habibi1, Vincent G DeMarco1, Dongqing Chen1

  • 1Department of Medicine-Endocrinology and Metabolism, University of Missouri School of Medicine, Columbia, MO 65212, USA; Harry S Truman Memorial Veterans Hospital, Research Service, 800 Hospital Dr, Columbia, MO 65201, USA.

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A Western diet promotes arterial stiffening by increasing CD36 in endothelial cells, leading to insulin resistance and vascular damage. Removing this CD36 protects against diet-induced aortic stiffening and related issues.

Keywords:
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Area of Science:

  • Cardiovascular Biology
  • Metabolic Diseases
  • Molecular Medicine

Background:

  • Western diets (WD) are linked to obesity, insulin resistance, and arterial stiffening, major cardiovascular disease risk factors.
  • Elevated CD36 expression correlates with ectopic lipid accumulation, insulin resistance, and arterial stiffening.
  • Endothelial cell-specific CD36 (ECCD36) role in WD-induced vascular dysfunction remains unclear.

Purpose of the Study:

  • To investigate the role of endothelial cell-specific CD36 (ECCD36) in Western diet-induced aortic insulin resistance, lipid accumulation, inflammation, fibrosis, remodeling, and stiffening.

Main Methods:

  • Female ECCD36 knockout and wild-type mice were fed WD or standard chow for 16 weeks.
  • Aortic stiffness assessed by pulse wave velocity; vascular function by wire myography.
  • Gene expression, lipid content, and aortic remodeling analyzed using molecular and histological techniques.

Main Results:

  • WD induced aortic stiffening, insulin resistance, and impaired insulin signaling (PI3K/Akt pathway).
  • WD-associated changes included mTOR/S6K activation, lipid dysregulation, reduced occludin, inflammation, and remodeling.
  • These WD-induced abnormalities were significantly attenuated in ECCD36 knockout mice.

Conclusions:

  • Heightened ECCD36 signaling under WD contributes to aortic insulin resistance, lipid accumulation, and endothelial dysfunction.
  • ECCD36 promotes inflammation, fibrosis, vascular remodeling, and arterial stiffening in response to a Western diet.
  • Targeting ECCD36 may offer a therapeutic strategy against diet-induced cardiovascular complications.