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Published on: April 1, 2015

Fibrin D-dimer fragments enhance inflammatory responses in macrophages: role in advancing atherosclerosis

Dong Zhou1, Peng-Yuan Yang, Bin Zhou

  • 1Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai, China.

Clinical and Experimental Pharmacology & Physiology
|January 26, 2007
PubMed

Insights

Fibrin D-dimer fragments promote atherosclerosis by enhancing inflammatory responses in macrophages. This study reveals D-dimer

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Biology

Background:

  • Fibrin D-dimer is a known cardiovascular disease risk marker.
  • Its specific role in macrophage foam cell formation during atherogenesis is not well understood.

Purpose of the Study:

  • To investigate the impact of fibrin D-dimer fragments on macrophage function in atherosclerosis.
  • To identify genes regulated by D-dimer fragments in atherosclerotic processes.

Main Methods:

  • Microarray analysis to assess gene expression changes in macrophages treated with D-dimer fragments.
  • SYBR real-time polymerase chain reaction to validate specific gene upregulation.

Main Results:

  • D-dimer fragments significantly upregulated 27 genes involved in key atherosclerotic pathways.
  • Validated upregulation of intercellular adhesion molecule-1, MMP-9, LOX-1, VEGF-A, and PPAR-α.
  • Confirmed a pro-atherosclerotic role of D-dimer in macrophage function.

Conclusions:

  • Fibrin D-dimer fragments enhance the inflammatory response in macrophages.
  • This contributes to macrophage-derived foam cell formation, a critical step in atherogenesis.
  • Provides direct evidence for D-dimer's pro-atherosclerotic effects on macrophage function.

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