This strain is an Ldlr deletion mouse model that uses gene editing technology to knock out the expression of human LDLR gene homolog in mice with impaired LDLR receptor synthesis, resulting in elevated serum cholesterol levels, which are further exacerbated by feeding on a high-fat diet (HFD), and the formation of aortic plaques. Homozygous Ldlr KO mice are viable and fertile and can be used for studies such as hypercholesterolemia and atherosclerosis.