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Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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Related Experiment Video

Updated: Nov 20, 2025

Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
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Targeting Macrophages in Atherosclerosis.

Dan Hu1, Zengyan Wang2, Yuzhong Wang3

  • 1Department of Cardiovasology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, China.

Current Pharmaceutical Biotechnology
|January 22, 2021
PubMed
Summary
This summary is machine-generated.

Macrophages are key inflammatory cells in atherosclerosis (AS), a major cause of cardiovascular disease. Understanding how these cells drive AS progression or regression offers new therapeutic targets.

Keywords:
Atherosclerosisimmunoreactioninflammationmacrophagespathogenesisregulatory mechanism.

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pathology

Background:

  • Atherosclerosis (AS) is a chronic inflammatory disease underlying Coronary Atherosclerotic Disease (CAD) and stroke.
  • Macrophages are central inflammatory cells in atherosclerotic lesions, critically influencing plaque development and regression.
  • Both pro-inflammatory and anti-inflammatory factors modulate macrophage behavior in AS.

Purpose of the Study:

  • To review the multifaceted roles of macrophages in the pathogenesis of atherosclerosis.
  • To elucidate the regulatory mechanisms by which macrophages influence AS development and progression.
  • To highlight macrophages as potential therapeutic targets for AS diagnosis and treatment.

Main Methods:

  • Literature review focusing on macrophage biology in atherosclerosis.
  • Analysis of pro-inflammatory and anti-inflammatory factor effects on macrophage polarization and function.
  • Synthesis of current understanding of macrophage-mediated lipid metabolism and plaque stability.

Main Results:

  • Pro-inflammatory factors promote M1 macrophage polarization, lipid accumulation, and foam cell formation, driving AS.
  • Anti-inflammatory factors induce M2 macrophage polarization, promoting tissue repair and plaque stabilization.
  • Macrophages regulate lipid metabolism and influence T-cell responses, impacting AS progression.

Conclusions:

  • Macrophages play a dual role in AS, with M1 promoting inflammation and M2 mediating resolution.
  • Targeting macrophage polarization and function presents a promising strategy for managing AS.
  • Further research into macrophage-centric mechanisms can yield novel diagnostic and therapeutic approaches for AS.