Inclusion of the EDA and EDB domains in cell-derived fibronectin is required for pro-inflammatory signaling.147 Thus, α5β1-fibronectin interactions create a positive feedback loop to maintain inflammation and promote leakage and atherosclerotic plaque formation, and blockade or haploinsufficiency of α5β1 reduces vascular leakage as well as formation of atherosclerotic lesions in mice.148. Here, FN1 is linked to Atherosclerotic lesion.