Taken together, these results provide evidence that SMC-derived cells within advanced mouse and human atherosclerotic lesions exhibit far greater phenotypic plasticity than generally believed, with Klf4 regulating transition to multiple phenotypes including Lgals3⁺ osteogenic cells likely to be detrimental for late-stage atherosclerosis plaque pathogenesis.
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Alencar et al. (2020) studied this question.
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