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Updated: Aug 5, 2025

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
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Surfactant protein A promotes atherosclerosis through mediating macrophage foam cell formation

Skylar D King, Dunpeng Cai, Mikayla M Fraunfelder

    Biorxiv : the Preprint Server for Biology
    |March 30, 2023
    PubMed
    Abstract

    Insights

    Surfactant protein A (SPA) promotes atherosclerosis by enhancing macrophage foam cell formation. SPA deficiency reduces cholesterol accumulation and lesion development, highlighting SPA as a therapeutic target for atherosclerosis.

    Area of Science:

    • Cardiovascular Biology
    • Immunology
    • Lipid Metabolism

    Background:

    • Atherosclerosis is an inflammatory disease driven by macrophage foam cells.
    • Surfactant protein A (SPA) regulates macrophage function but its role in atherosclerosis is unknown.

    Approach:

    • Assessed SPA's role in macrophage foam cell formation using wildtype and SPA-deficient mice.
    • Examined SPA expression in human and mouse atherosclerotic tissues.
    • Investigated atherosclerosis development in vivo in hypercholesteremic mice.

    Key Points:

    • SPA deficiency reduced intracellular cholesterol and foam cell formation in vitro.
    • SPA deficiency decreased CD36 expression, a key scavenger receptor.
    • SPA expression was elevated in atherosclerotic lesions.
    • SPA deficiency attenuated atherosclerosis in vivo.

    Conclusions:

    • SPA is a novel factor in atherosclerosis development.
    • SPA promotes atherosclerosis by increasing scavenger receptor CD36 expression.
    • Targeting SPA may offer a new therapeutic strategy for atherosclerosis.

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