Animal models of atherosclerosis

Table 1 Animal models and their features

Model	Features	Ref.
Mice
Apo E-/- mice	Develops spontaneous atherosclerosis, associated with elevated levels of circulating cholesterol-rich VLDL particles	Zhang et al[3]
LDL receptor deficient KO mice	This model needs dietary cholesterol to develop hypercholesterolemia and atherosclerosis- associated with elevated levels of circulating cholesterol-rich LDL and VLDL particles	Sanan et al[16]
Apo E*3-Leiden transgenic mice	This model needs dietary cholesterol to develop hypercholesterolemia and atherosclerosis-associated with elevated levels of circulating cholesterol	Groot et al[24] van Vlijmen et al[25]
Hepatic lipase-KO mice	This 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 mice	This 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 mice	This model has reported to have decreased HDL cholesterol levels with variable degree of atherosclerosis	Föger et al[19]
Cross breeding of human apo B100 transgenic mice with LDL receptor deficient mice	This model develops severe hypercholesterolemia and atherosclerosis	Sanan 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 stress	Lewis et al[27]
Surgical model of apo E-/- mice	A mouse model for studying unstable/ruptured atherosclerotic plaques	Chen et al[28]
Animal model developed using bone marrow technique	Apo E-KO mice model with and without deficiency of CCR2	Ishibashi et al[30]
Rabbits
WHHL	Naturally deficient in LDL receptors resembling human familial hypercholesterolemia	Watanabe[10]
STH	Rabbit model for human hypertriglyceridemia and combined hyperlipidemia	Beaty et al[38]
NZW-human apo B100 transgenic rabbits	Transgenic animal model manifesting combined hyperlipidemia with reduced HDL-cholesterol concentrations	Fan et al[33]
NZW-human apo AI or human LCAT transgenic rabbits	Rabbit model with elevated HDL-cholesterol levels and reduced atherosclerosis	Duverger et al[34]
Pigs
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 monkeys	Develops spontaneous atherosclerosis. This animal model develops majority of atherosclerotic lesions in the anterior descending and circumflex branches of the left coronary artery	Carey[45]
Cebus monkeys	Develops spontaneous atherosclerosis. This animal model develops atherosclerotic lesions in their carotid bifurcation and coronary arteries	Carey[45]
Cynomolgus monkeys and African green monkeys	These monkeys develop spontaneous atherosclerosis. Atherosclerotic lesions being developed in coronary arteries and abdominal aorta, respectively	Hollander et al[49]
Others
Dogs Hamsters Guinea pigs Birds	These animal models have significant amount of limitations that have not extensively used	Geer et al[50] Nistor et al[52] Fernandez et al[54] Wagner et al[56]

Apo E^-/-: Apolipoprotein E deficient; KO: Knockout; VLDL: Very low density lipoprotein; LDL: Low density lipoprotein; HDL: High density lipoprotein; CETP: Cholesterol-ester transfer protein; LCAT: Lecithin cholesterol acyl transferase; CCR2: Chemoattractant protein-1 receptor, CCR2; WHHL: Watanabe Heritable Hyperlipidemic; STH: St. Thomas’ Hospital; NZW: New Zealand White.