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Numerous cysteine-based redox switches have been found to underpin many different signalling systems and regulate physiological outputs across kingdoms 22,23
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]
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