Chemokines control mobilization, recruitment, and fate of monocytes in atherosclerosis

Maik Drechsler1, Johan Duchene2, Oliver Soehnlein1

  • 1From the Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany (M.D., J.D., O.S.); Department of Pathology, Academic Medical Center Amsterdam, University of Amsterdam, Amsterdam, The Netherlands (M.D., O.S.); and German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany (M.D., O.S.). maik.drechsler@med.uni-muenchen.de oliver.soehnlein@gmail.com.

Insights

Chemokines and their receptors control monocyte movement, which is crucial for atherosclerosis development. Understanding this interplay aids in developing treatments for this chronic inflammatory artery disease.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Inflammation Research

Background:

  • Atherosclerosis is a chronic inflammatory disease affecting large arteries.
  • It involves monocyte infiltration, macrophage accumulation, and foam cell formation.
  • Chemokines and their receptors are key regulators of immune cell trafficking.

Purpose of the Study:

  • To review the current understanding of monocyte-chemokine interactions in atherosclerosis.
  • To highlight the role of these interactions in disease development, progression, and regression.

Main Methods:

  • Literature review of studies on monocyte trafficking and chemokines in atherosclerosis.
  • Synthesis of current knowledge on chemokine receptor signaling in monocytes.
  • Analysis of the impact of chemokines on macrophage differentiation and function.

Main Results:

  • Chemokines precisely regulate monocyte recruitment to the arterial wall.
  • Specific chemokine pathways are critical at different stages of atherosclerosis.
  • Targeting chemokine pathways offers potential therapeutic strategies.

Conclusions:

  • Monocyte-chemokine axis is central to atherosclerosis pathogenesis.
  • Further research into these interactions can reveal novel therapeutic targets.
  • Modulating chemokine signaling may impact atherosclerosis progression and regression.

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