Copyright ©2014 Baishideng Publishing Group Inc.
World J Clin Cases. May 16, 2014; 2(5): 126-132
Published online May 16, 2014. doi: 10.12998/wjcc.v2.i5.126
Table 1 Animal models and their features
Apo E-/- miceDevelops spontaneous atherosclerosis, associated with elevated levels of circulating cholesterol-rich VLDL particlesZhang et al[3]
LDL receptor deficient KO miceThis model needs dietary cholesterol to develop hypercholesterolemia and atherosclerosis- associated with elevated levels of circulating cholesterol-rich LDL and VLDL particlesSanan et al[16]
Apo E*3-Leiden transgenic miceThis model needs dietary cholesterol to develop hypercholesterolemia and atherosclerosis-associated with elevated levels of circulating cholesterolGroot et al[24] van Vlijmen et al[25]
Hepatic lipase-KO miceThis model lacks hepatic lipase and develops elevated levels of plasma cholesterol, phospholipids, and HDL cholesterol and can be used for the study of HDL metabolism.Homanics et al[17]
Human apo B100 transgenic miceThis mice model, associated with substantial increased level of LDL cholesterol level and useful for studying various aspects of lipoprotein metabolism and for further delineating the role of LDL in atherogenesis.Greeve et al[18]
Human CETP transgenic miceThis model has reported to have decreased HDL cholesterol levels with variable degree of atherosclerosisFöger et al[19]
Cross breeding of human apo B100 transgenic mice with LDL receptor deficient miceThis model develops severe hypercholesterolemia and atherosclerosisSanan et al[16]
Cross breeding of human LCAT transgenic mice with CETP transgenic mice.A mouse model with low total cholesterol levels and reduced atherosclerosis burden.Föger et al[19]
Apo E/GPx1 double knockout (apo E-/- GPx1-/-)This model features combined hyperlipidemia and hyperglycemia with increased oxidative stressLewis et al[27]
Surgical model of apo E-/- miceA mouse model for studying unstable/ruptured atherosclerotic plaquesChen et al[28]
Animal model developed using bone marrow techniqueApo E-KO mice model with and without deficiency of CCR2Ishibashi et al[30]
WHHLNaturally deficient in LDL receptors resembling human familial hypercholesterolemiaWatanabe[10]
STHRabbit model for human hypertriglyceridemia and combined hyperlipidemiaBeaty et al[38]
NZW-human apo B100 transgenic rabbitsTransgenic animal model manifesting combined hyperlipidemia with reduced HDL-cholesterol concentrationsFan et al[33]
NZW-human apo AI or human LCAT transgenic rabbitsRabbit model with elevated HDL-cholesterol levels and reduced atherosclerosisDuverger et al[34]
Lipoprotein-associated mutations (designated Lpb5, Lpr1, and Lpu1)This pig model develops hypercholesterolemia and atherosclerosis without dietary cholesterol. In addition to coronary arteries, iliac and femoral arties also develop atherosclerotic lesions which become complicated by 2 year of age.Prescott et al[44]
Non-human primates
Rhesus monkeysDevelops spontaneous atherosclerosis. This animal model develops majority of atherosclerotic lesions in the anterior descending and circumflex branches of the left coronary arteryCarey[45]
Cebus monkeysDevelops spontaneous atherosclerosis. This animal model develops atherosclerotic lesions in their carotid bifurcation and coronary arteriesCarey[45]
Cynomolgus monkeys and African green monkeysThese monkeys develop spontaneous atherosclerosis. Atherosclerotic lesions being developed in coronary arteries and abdominal aorta, respectivelyHollander et al[49]
Dogs Hamsters Guinea pigs BirdsThese animal models have significant amount of limitations that have not extensively usedGeer et al[50] Nistor et al[52] Fernandez et al[54] Wagner et al[56]