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When the vascular wall is stimulated by hypoxia, mechanical damage, or platelet-derived growth factor (PDGF-BB), the transcription coactivator MYOCD and the nuclear transcription factor EIkI compete for the same binding site on the serum response factor, and the contractile phenotype-responsive SRF-MYOCD complex is converted to the synthetic phenotype-responsive SRF-ELK1 complex, prompting the VSMCs to transform from a contractile phenotype to a synthetic phenotype [43, 44]