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Published on: April 3, 2017

Macrophages: an elusive yet emerging therapeutic target of atherosclerosis

R L Tiwari1, V Singh, M K Barthwal

  • 1Division of Pharmacology, Central Drug Research Institute, Lucknow 226001, India.

Medicinal Research Reviews
|November 16, 2007
PubMed

Insights

Macrophages are key in atherosclerosis development and progression, making them ideal therapeutic targets. Targeting macrophage functions like lipid uptake and inflammation offers promising strategies for treating this cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Cell Biology

Background:

  • Macrophages play a critical role in the initiation and progression of atherosclerosis.
  • Key processes include monocyte recruitment, foam cell formation, and inflammatory responses.
  • Dysfunctional macrophages contribute to plaque vulnerability and rupture.

Purpose of the Study:

  • To review the multifaceted roles of macrophages in atherosclerosis.
  • To highlight macrophage-derived molecules and pathways as potential therapeutic targets.
  • To emphasize the importance of understanding macrophage biology for developing novel treatments.

Main Methods:

  • Literature review of macrophage involvement in atherosclerosis.
  • Analysis of molecular mechanisms in macrophage lipid metabolism and inflammation.
  • Examination of cellular processes like proliferation and apoptosis in macrophages.
  • Identification of specific receptors, signaling pathways, and enzymes as therapeutic targets.

Main Results:

  • Cell adhesion molecules, scavenger receptors (SR-A, CD-36), and nuclear receptors (PPAR, LXR) are crucial for monocyte recruitment and foam cell formation.
  • Cholesterol metabolism proteins (ABCA1, ABCG1, ACAT, ApoA-1, NCEH) and signaling pathways (MAPK) are implicated in foam cell development.
  • Macrophage proliferation, apoptosis, endoplasmic reticulum stress, and free radical interactions influence plaque stability.
  • Matrix metalloproteinases (MMPs) contribute to plaque weakening and rupture.
  • Polymorphisms in genes like CD-14, TLR-4, LOX-1, ALOX-15, and Connexin37 are associated with macrophage dysfunction in atherosclerosis.

Conclusions:

  • Macrophages are central regulators of atherosclerosis through lipid metabolism, inflammation, and plaque remodeling.
  • Targeting specific macrophage pathways, receptors, and molecules presents viable therapeutic strategies.
  • Further research into macrophage biology is essential for advancing atherosclerosis treatment.

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