. 2016 May 5;7(30):48788–48812. doi: 10.18632/oncotarget.9195

Table 1. The role of STATs and IRFs in CVD.

Transcription factor	Contribution to CVD development	References
STAT1	Foam-cell formation, atherosclerotic lesion development, MC apoptosis, VSMCs de-differentiation and proliferation, neointimal hyperplasia, elevated expression of chemokines, promotion of oxidative stress and tissue injury.	[74, 87–91]
STAT2	Regulation of type I IFN signaling and gene expression.	[92]
STAT3	VSMCs de-differentiation, lesion formation, recruitment of inflammatory cells to the vessel wall.	[93, 94]
IRF1	Protection against neointima formation, iNOS activation in response to stress conditions, increased ventricular dilation and fibrosis, acceleration of vascular remodeling, exacerbation of ischaemic stroke.	[97–100]
IRF8	Cells proliferation, neointima and lesion formation, association of IRF8 gene polymorphism with coronary heart disease in SLE, elevated expression in response to mechanical injury of the artery, VSMCs phenotypic switching, induction of M1 phenotype in MC, negative regulator of pathological cardiac hypertrophy.	[100–102, 105]