LDLR and atherosclerosis: In CHOP-deficient murine models of atherosclerosis, such as fat-fed Chop+/+;Apoe−/− and Chop−/−;Apoe−/− mice, as well as fat-fed Chop−/−;Ldlr−/− versus Chop+/+;Ldlr−/− mice, reductions in lesion area due to substantial reduction of plaque necrosis and intimal apoptosis have been associated with deficits in CHOP protein [11].