LDLR and atherosclerosis: Blockade of DLL4-Notch signaling with an anti-DLL4 mAb decreased accumulation of macrophage, diminished calcification of plaque, reduced insulin resistance, and inhibited progression of atherosclerosis in Ldlr−/− mice.260 Since the Notch signaling is a potentially attractive target candidate in atherosclerosis, further research is needed to elucidate the distinct biological roles of Notch receptors and ligands in the plaque progression and to validate the individual potentials as novel therapeutic strategies.256