Abstract:Vascular smooth muscle is well known for phenotype plasticity and upon injury or in response to disease it modulates from a contractile phenotype to a sythetic phenotype that contributes to vascular remodeling. We have demonstrated that increased expression of CaMKII is associated with modulation of VSM to the synthetic phenotype but there is very little direct evidence indicating a function for the kinase in regulating VSM cell gene transcription. Herein, we report that the transcriptional co‐repressors HDAC4… Show more
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