RIV enhances cellular viability under conditions of hypoxia by suppressing the protease-activated receptor 2 signaling pathway; it diminishes the expression of molecules associated with inflammation and fibrosis in cardiac fibroblasts, thereby reducing the incidence of aortic atherosclerosis and coronary artery occlusion, and it significantly mitigates cardiac fibrosis [25]. Here, F2RL1 is linked to aortic atherosclerosis.