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Macrophage Migration Inhibitory Factor (MIF)-Based Therapeutic Concepts in Atherosclerosis and Inflammation

Dzmitry Sinitski1, Christos Kontos2, Christine Krammer1

  • 1Department of Vascular Biology, Institute for Stroke and Dementia Research (ISD), Klinikum der Universität München (KUM), Ludwig-Maximilians-University (LMU), Munich, Germany.

Thrombosis and Haemostasis
|February 5, 2019
PubMed

Insights

Macrophage migration inhibitory factor (MIF) drives atherosclerosis by promoting inflammation and leukocyte recruitment. Targeting MIF offers a novel therapeutic strategy for cardiovascular disease, distinct from traditional chemokine pathways.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Molecular Biology

Background:

  • Chemokines are key in leukocyte recruitment for atherosclerosis, but their complex network limits therapeutic blockade.
  • Macrophage migration inhibitory factor (MIF) is a critical mediator in atherosclerotic lesion development.
  • MIF acts as both an inflammatory cytokine and an atypical chemokine, interacting with CXCR2 and CXCR4.

Purpose of the Study:

  • To review the therapeutic potential of targeting MIF in atherosclerosis.
  • To analyze the pros and cons of anti-MIF protein strategies.
  • To discuss MIF's molecular characteristics and receptor specificities in cardiovascular disease.

Main Methods:

  • Review of existing literature on MIF, chemokines, and atherosclerosis.
  • Analysis of MIF's dual role as an inflammatory mediator and cardioprotective factor.
  • Examination of therapeutic approaches targeting MIF, including small molecules, antibodies, and peptides.

Main Results:

  • MIF promotes atherogenic leukocyte recruitment and inflammation via CXCR2/CXCR4.
  • MIF also exhibits CD74-mediated cardioprotective effects in specific phases.
  • MIF and MIF-2/D-DT present unique therapeutic opportunities for atherosclerosis.

Conclusions:

  • Targeting MIF offers a promising, potentially selective anti-atherosclerotic strategy.
  • Anti-MIF therapies may bypass the limitations of targeting classical chemokine pathways.
  • Further research into MIF-based approaches is warranted for cardiovascular disease treatment.

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