GSE184391
BACH1 Deficiency Prevents Neointima Formation and Maintains the Differentiated Phenotype of Vascular Smooth Muscle Cell by Regulating Chromatin Accessibility
Chromatin accessibility is important for cell fate determination in differentiation and multiple pathophysiological processes. Here, we report a transcription factor BACH1, facilitates the recruitment of G9a and YAP, maintains the state of H3K9me2 and decreases the chromatin accessibility at the promoter of VSMC marker genes, thereby repressing their expression and contributing to dedifferentiated VSMC phenotype. Moreover, VSMC-specific loss of BACH1 in mice inhibited the transformation of VSMC from contractile to synthetic phenotype and VSMC proliferation and attenuated the neointimal hyperplasia in wire-injured femoral arteries. Overall design: BACH1