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Joseph L Witztum1

  • 1Department of Medicine, University of California San Diego, La Jolla, California 92093, USA. jwitztum@ucsd.edu

The Journal of Clinical Investigation
|August 3, 2005
PubMed

Insights

Macrophage scavenger receptors like CD36 and SR-A are key in foam cell formation. However, studies show deleting these receptors did not reduce atherosclerosis in mice, leaving their role unresolved.

Area of Science:

  • Immunology
  • Cardiovascular Research
  • Molecular Biology

Background:

  • Macrophage scavenger receptors, including CD36 and scavenger receptor class A (SR-A), are implicated in foam cell formation.
  • These receptors are believed to mediate the uptake of oxidized low-density lipoprotein (LDL), a critical step in atherogenesis.

Purpose of the Study:

  • To investigate the role of CD36 and SR-A in the development of atherosclerosis.
  • To reconcile conflicting findings regarding the contribution of these scavenger receptors to atherogenesis.

Main Methods:

  • Utilizing apolipoprotein E-deficient (Apoe) mice lacking either the CD36 or SR-A receptor.
  • Assessing atherosclerosis development, specifically at the aortic valve level, in knockout mice compared to wild-type controls.

Main Results:

  • Apoe mice deficient in CD36 or SR-A did not exhibit reduced atherosclerosis at the aortic valve compared to wild-type Apoe mice.
  • These findings contrast with previous studies that reported decreased atherogenesis upon deletion of these receptors.

Conclusions:

  • The precise role of CD36 and SR-A in atherogenesis remains uncertain.
  • Discrepancies in study outcomes suggest a complex interplay of factors influencing the contribution of these receptors to the disease process.

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