Apolipoprotein E knock-out and knock-in mice: atherosclerosis, metabolic syndrome, and beyond

Area of Science:

• Cardiovascular Science
• Metabolic Disease Research
• Genetics and Complex Diseases

Background:

• Atherosclerosis is primarily a human disease, making animal models crucial for research.
• Apolipoprotein E-deficient (apoEKO) mice have emerged as a key model for studying atherogenesis.
• Previous understanding of apoE focused on lipoprotein metabolism, but recent findings suggest broader roles.

Purpose of the Study:

• To highlight the utility of apoEKO mice in modeling human atherosclerosis.
• To explore the role of apoE in energy metabolism beyond lipoprotein regulation.
• To investigate the impact of genetic alterations in apoE on complex disease pathogenesis.

Main Methods:

• Utilizing apolipoprotein E-deficient (apoEKO) mice to study atherosclerosis.
• Employing knockin mice expressing human apoE isoforms for comparative genetic studies.
• Analyzing data on plaque formation, adiposity, and glucose homeostasis in mouse models.

Main Results:

• ApoEKO mice effectively model human-like atherosclerotic plaques.
• ApoE deficiency is associated with reduced adiposity and improved glucose homeostasis.
• Genetic variations in apoE influence disease development in interaction with environmental factors.

Conclusions:

• ApoEKO mice provide a robust platform for investigating atherosclerosis and potential therapies.
• ApoE plays a significant role in energy metabolism in peripheral tissues.
• Mouse models, including apoEKO and human apoE knockin mice, are essential for understanding complex human diseases.