Review Article
Roles of the WHHL Rabbit in Translational Research on Hypercholesterolemia and Cardiovascular Diseases
Table 1
Comparison of lipid metabolism, atherosclerosis, and cardiac functions between genetically modified mice and WHHLMI rabbits.
| | Genetically modified mice | WHHLMI rabbits |
| Lipid metabolism | | | Major lipoprotein in the blood | X (Chylomicron, VLDL) | O (LDL) | Structural protein in theendogenous lipoprotein | X (apoB48) | O (apoB100) | Expression of apoB editing enzyme | X (The small intestine, liver) | O (The small intestine) | CETP activity in the blood | X (No) | O (Exists) | Hepatic lipase | X (Released to circulation) | O (Bound to vessel membrane) | Atherosclerosis | | | The coronary lesion | X (Resistant) | Δ (Spontaneously develops) | Composition of the lesions | X (Over accumulation of macrophages) | O (Various lesions) | VLDL receptor | X (no expression) | O (expression) | Heart | | | Electrocardiogram | | | Limb lead | X (Largely different waveforms) | O (Similar to humans) | Chest lead | X (Difficult to monitor) | O (Similar to humans) | Myocardial ion channel | X (Ito and IK,slow) | O (Ikr and IKs) | Myocardial fibers | X (α-myosin heavy chain) | O (β-myosin heavy chain) | Others | | | Inflammatory markers | X (SAP) | O (CRP) | The hypocholesterolemic effect of statins | X (Resistant) | O (Effective) |
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O: similar to humans; Δ: partly similar to humans; X: largely different from humans.
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