TCF21 and the environmental sensor aryl-hydrocarbon receptor cooperate to activate a pro-inflammatory gene expression program in coronary artery smooth muscle cells
Fig 9
Schematic representation of AHR-TCF21 interactions that may modulate the effect of environmental stimuli on the progression of inflammation and atherosclerotic plaque formation.
Environmental toxins, including dioxin and tobacco, as well as endogenous activators such as ox-LDL activate the AHR pathway, leading to increased inflammatory burden in the plaque. TCF21 can further increase the burden by increasing AHR expression as well as interacting with AHR at its downstream genes.