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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
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Colchicine promotes atherosclerotic plaque stability independently of inflammation

Weizhen Li, Alexander Lin, Michael Hutton

    Biorxiv : the Preprint Server for Biology
    |October 24, 2023
    PubMed

    Insights

    Colchicine reverses atherosclerosis plaque by converting harmful cells into protective ones, stabilizing artery walls. This novel mechanism, independent of anti-inflammatory effects, targets smooth muscle cell phenotype for plaque regression.

    Area of Science:

    • Cardiovascular Research
    • Cell Biology
    • Pharmacology

    Background:

    • Atherosclerosis is a chronic inflammatory disease involving vascular smooth muscle cell (SMC) trans-differentiation.
    • Current therapies do not reverse detrimental SMC-derived cell phenotypes, hindering plaque regression and patient outcomes.

    Approach:

    • Investigated colchicine's role in modulating SMC-derived cell phenotype beyond its anti-inflammatory effects.
    • Utilized SMC fate mapping in an advanced atherosclerotic lesion model.
    • Examined the dependency on Notch3 signaling in SMC-derived plaque cells.

    Key Points:

    • Colchicine induced plaque regression by converting pathogenic SMC-derived cells (macrophage-like, osteoblast-like) into protective myofibroblast-like cells.
    • This conversion led to fibrous cap thickening and stabilization.
    • The observed effects were dependent on Notch3 signaling within SMC-derived plaque cells.

    Conclusions:

    • Colchicine demonstrates a novel mechanism for promoting atherosclerotic plaque regression by beneficially modulating SMC phenotype.
    • Targeting SMC phenotype via Notch3 signaling offers a new therapeutic strategy for atherosclerosis, complementing anti-inflammatory approaches.
    • Findings may explain colchicine's clinical efficacy in atherosclerosis treatment.

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