Our group previously established an endothelial cell-specific CXCR4 knockout (EC CXCR4 KO) mouse model, which spontaneously develops AS accompanied by significant functional impairment, including elevated aortic valve peak velocity, increased pressure gradient, ventricular hypertrophy, and reduced ejection fraction [26]. Here, CXCR4 is linked to Ventricular hypertrophy.