Table 3.

Genetically modified animal models for atherosclerosis.

Experimental model	Description
Apolipoprotein E knockout (ApoE−/−) mice	Apolipoprotein E (apoE), a constituent of lipoprotein responsible for packaging cholesterol and other fats and carrying them through the bloodstream, is inactivated by gene targeting. They exhibit a higher total plasma cholesterol concentration of 11 mM compared to 2 mM in their parent C57BL/6 mice [114].
LDL receptor knockout (LDLR−/−) mice	LDL receptor (LDLR) is a cell surface receptor in liver cells that mediates the endocytosis of apoE to clear cholesterol-abundant LDL particles from the circulation. Total plasma cholesterol levels increase twofold compared to those of wild-type, owing to a seven- to ninefold increase in intermediate density lipoproteins (IDL) and LDL without a significant change in HDL [115].
Scavenger receptor class B member 1 knockout (SR-BI KO) mice	Scavenger receptor class B member 1 (SR-BI) functions in facilitating the uptake of cholesterol from HDL in the liver. It plays a key role in determining the levels of plasma cholesterol (primarily HDL). Heterozygous and homozygous mutants show 31% and 125% increase, respectively, in plasma cholesterol concentrations than wild-types [116].
db/db mice	OB-R is a high affinity receptor for leptin, an important circulating signal for the regulation of feeding, appetite, and body weight. Fatty acid oxidation rates are progressively higher in db/db mice in parallel with the earlier onset and greater duration of hyperglycemia [117].
ob/ob mice	A mutation results in a structurally defective leptin that does not bind to the OB-R. Mice that are ob/ob have no leptin action and exhibit obesity and endothelial dysfunction [118].
Fatty Zucker rats	A spontaneous mutant gene (fa or fatty) that affects the action of the leptin. They have high levels of lipids and cholesterol in their bloodstream and become noticeably obese by 3 to 5 weeks of age and over 40% lipid of their body composition by 14 weeks of age [119].
Cholesterol ester transfer protein (CETP) transgenic rats	CETP inhibits HDL-mediated reverse cholesterol transport by transferring cholesterol from HDL to very low-density lipoprotein (VLDL) and LDL, promoting atherogenesis. The animals exhibit 82% increase in non-HDL cholesterol in addition to 80% reduction in HDL cholesterol when compared to wild-type rats [120].

HDL: high-density lipoprotein; LDL: low-density lipoprotein.