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DPP-4 inhibition ameliorates atherosclerosis by priming monocytes into M2 macrophages

C Brenner1, W M Franz2, S Kühlenthal3

  • 1Department of Internal Medicine III, Medical University of Innsbruck, Innsbruck, Austria; Department of Internal Medicine I, University of Munich, Munich, Germany.

International Journal of Cardiology
|July 22, 2015
PubMed
Abstract

Insights

Sitagliptin, a DPP-4 inhibitor, reduces atherosclerosis by promoting M2 macrophage polarization through SDF-1/CXCR4 signaling. This suggests gliptins may be effective in preventing atherosclerosis.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pharmacology

Background:

  • Dipeptidyl peptidase-4 (DPP-4) inhibitors (gliptins) are used for type 2 diabetes.
  • Animal studies suggest gliptins have anti-atherosclerotic effects, but clinical data is mixed.
  • The role of SDF-1/CXCR4 signaling in gliptin's vascular effects requires clarification.

Purpose of the Study:

  • To investigate the mechanism of gliptin's anti-atherosclerotic action.
  • To determine the role of SDF-1/CXCR4 signaling in gliptin-mediated effects on atherosclerosis.
  • To evaluate the potential of gliptin therapy in atherosclerosis prevention.

Main Methods:

  • ApoE-/- mice on a high-cholesterol diet were treated with Sitagliptin.
  • Flow cytometry analyzed macrophage populations (M1/M2) in aortic plaques.
  • CXCR4/SDF-1 signaling was blocked using AMD3100.

Main Results:

  • Sitagliptin significantly reduced atherosclerotic plaque load in mouse aortas.
  • Gliptin therapy increased M2 macrophage (CD206+) accumulation in aortic walls.
  • CXCR4/SDF-1 blockade negated Sitagliptin's anti-atherosclerotic effects and M2 macrophage enrichment.
  • Sitagliptin promoted M2 polarization of macrophages.

Conclusions:

  • Sitagliptin inhibits early atherosclerosis by inducing M2 macrophage polarization via SDF-1/CXCR4 signaling.
  • Gliptin therapy may be particularly effective for atherosclerosis prevention.
  • Understanding this mechanism could refine gliptin's therapeutic application in cardiovascular disease.
Keywords:
AtherosclerosisM2 macrophagesPrimingSDF-1Sitagliptin

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