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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
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Foam cells in atherosclerosis

Xiao-Hua Yu1, Yu-Chang Fu, Da-Wei Zhang

  • 1Life Science Research Center, University of South China, Hengyang, Hunan 421001, China.

Clinica Chimica Acta; International Journal of Clinical Chemistry
|June 21, 2013
PubMed

Insights

Macrophage foam cell formation in atherosclerosis involves an imbalance in cholesterol processes. Understanding cholesterol uptake, esterification, and efflux is key to developing new treatments for this chronic arterial disease.

Area of Science:

  • Cardiovascular Biology
  • Cellular Metabolism
  • Atherosclerosis Research

Background:

  • Atherosclerosis is a chronic disease driven by cholesterol buildup in arteries.
  • Macrophage foam cells are central to atherosclerosis development, arising from cholesterol imbalance.
  • Key processes include cholesterol uptake, esterification, and efflux within macrophages.

Purpose of the Study:

  • To review the mechanisms of cholesterol uptake, esterification, and release in macrophages.
  • To highlight the roles of specific proteins in macrophage cholesterol homeostasis.
  • To provide a foundation for novel therapeutic strategies against atherosclerosis.

Main Methods:

  • This review synthesizes existing knowledge on macrophage cholesterol metabolism.
  • It examines the functions of key proteins involved in cholesterol transport and modification.
  • Literature review focusing on molecular mechanisms of foam cell formation.

Main Results:

  • CD36 and scavenger receptor class A (SR-A) mediate cholesterol uptake.
  • Acyl coenzyme A:cholesterol acyltransferase-1 (ACAT1) and neutral cholesteryl ester hydrolase (nCEH) regulate cholesterol esterification.
  • ATP-binding cassette transporters (ABCA1, ABCG1) and scavenger receptor BI (SR-BI) are critical for cholesterol efflux.

Conclusions:

  • Dysregulation of cholesterol influx, esterification, and efflux leads to macrophage foam cell formation.
  • Understanding these mechanisms is crucial for developing targeted therapies for atherosclerosis.
  • Further research into macrophage cholesterol pathways may yield novel treatment interventions.

Keywords:
ABCA1ABCG1ACAT1AGEATP-binding cassette transporter A1ATP-binding cassette transporter G1AtherosclerosisCD36CEERK1/2FCFoam cellsHDLLDLRLXRMAPKPI3KPKBPKCPPAR response elementsPPAR-γPPREsRCTRXRSR-ASR-BITGF-βacyl coenzyme A:cholesterol acyltransferase-1advanced glycation end productsapoA-IapoEapolipoprotein A-Iapolipoprotein Echolesterol esterextracellular signal-regulated kinases 1 and 2free cholesterolhigh-density lipoproteinliver X receptorlow-density lipoprotein receptormitogen-activated protein kinasenCEHneutral cholesteryl ester hydrolaseox-LDLoxidized low-density lipoproteinperoxisome proliferator-activated receptor-γphosphatidylinositol 3-kinaseprotein kinase Bprotein kinase Cretinoid X receptorreverse cholesterol transportscavenger receptor BIscavenger receptor class Atransforming growth factor-β

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