BACH1 Deficiency Prevents Neointima Formation and Maintains the Differentiated Phenotype of Vascular Smooth Muscle Cells by Regulating Chromatin Accessibility

Investigators explored the role of the transcription factor BTB and CNC homology 1 (BACH1) in vascular remodeling and its underlying mechanisms. BACH1 was highly expressed in human atherosclerotic plaques and had high transcriptional factor activity in vascular smooth muscle cells of human atherosclerotic arteries.