In conclusion, we demonstrate for the first time that plasma cholesterol in LDLR+/− hamsters can be significantly modulated by dietary cholesterol, which was highly associated with severity of atherosclerosis in the aorta and coronary arteries, suggesting that, compared to other heterozygous animal models with LDLR deficiency, the LDLR+/− hamster will display a great advantage in the study of diet-induced hyperlipidemia, atherosclerosis-related CHD, and the high-throughput screening of drugs targeting LDLR in future. The gene discussed is LDLR; the disease is coronary artery disorder.