Genome-wide association studies (GWAS) in coronary artery disease have revealed gene variants highly expressed in vascular smooth muscles cells (SMCs). Research now suggests that loss of one, Prdm16, drives a switch toward a synthetic SMC phenotype, with robust, potentially protective extracellular matrix production and fibrous cap formation.
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Acknowledgements
This work was supported by the US National Institutes of Health (HL115141, HL167905, HL171239, HL134849, DK142281 to M.W.F.; HL149999, DK107239, HL127118-02, DI-2021C1-22309, Arbor Way Foundation to J.P.) and the American Heart Association (20SFRN35200163 to M.W.F.).
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Feinberg, M.W., Plutzky, J. Flipping the PRDM16 switch in ‘multifunctional mesenchymes’ may help to define atherosclerotic plaque. Nat Cardiovasc Res 4, 1459–1461 (2025). https://doi.org/10.1038/s44161-025-00743-w
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DOI: https://doi.org/10.1038/s44161-025-00743-w