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Updated: Oct 1, 2025

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Macrophage SR-B1 in atherosclerotic cardiovascular disease

Thierry Huby1, Wilfried Le Goff

  • 1Sorbonne Universités, INSERM, Institute of Cardiometabolism and Nutrition (ICAN), UMR_S1166, Paris, France.

Current Opinion in Lipidology
|March 8, 2022
PubMed

Insights

Scavenger receptor class B type 1 (SR-B1) plays a key role in protecting against atherosclerosis by influencing macrophage function and promoting plaque stability, suggesting it as a potential therapeutic target.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Molecular Biology

Background:

  • Scavenger receptor class B type 1 (SR-B1) is known for its role in hepatic HDL metabolism and reverse cholesterol transport.
  • Emerging evidence suggests SR-B1 also exerts atheroprotective effects through non-hepatic mechanisms, particularly within macrophages.

Purpose of the Study:

  • To review and elucidate the non-hepatic mechanisms by which SR-B1 influences macrophage function in atherosclerosis.
  • To highlight the stage-dependent roles of SR-B1 in atherogenesis and its therapeutic potential.

Main Methods:

  • Review of recent scientific literature focusing on SR-B1's role in macrophage biology and atherosclerosis.
  • Analysis of studies investigating SR-B1's impact on efferocytosis, apoptosis, autophagy, and plaque stability.

Main Results:

  • SR-B1 promotes efferocytosis and free cholesterol-induced apoptosis of macrophages via apoptosis inhibitor of macrophage (AIM) in early lesions.
  • In advanced lesions, macrophage SR-B1 facilitates the clearance of apoptotic cells and induces autophagy, limiting necrotic core formation.
  • SR-B1 enhances plaque stability and contributes to atheroprotection in a manner dependent on the stage of atherosclerotic lesion development.

Conclusions:

  • SR-B1 plays a critical, stage-specific role in macrophage function during atherogenesis, extending beyond its hepatic functions.
  • Targeting macrophage SR-B1 presents a promising therapeutic strategy for cardiovascular disease.
Abstract

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