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Updated: Mar 7, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Comparative transcriptomic analysis of mice liver treated with different AMPK activators in a mice model of
Ang Ma1,2, Dongmei Wang1, Yuanyuan An1
1State Key Laboratory for Bioactive Substances and Functions of Natural Medicines, Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, China.
Abstract:
Atherosclerosis is known to be the primary underlying factor responsible for the development of cardiovascular diseases. Suppression of AMP-activated protein kinase stimulates arterial deposition of excess lipids, resulting in the development of atherosclerotic lesions. In this study we successfully developed the disease model of mice and mimicked the therapeutic effect, for that we chose three different AMP-activated protein kinase activators (IMM-H007, A-769662 and Metformin) to identify which one has a superior effect in the atherosclerosis model. We combined the transcriptomes of four groups of mice liver including high-fat diet group and the experimental groups treated with different AMP-activated protein kinase activators. We analyzed the increased genes to candidate metabolic and disease pathways. Compared to the high-fat diet group, a total of 799 differentially expressed genes were identified in treatment groups. There were 291, 473, and 323 differentially expressed genes in H007, Metformin, and A-769662 group respectively. And seven statistically significant pathways were observed in both H007 and Metformin groups. We expect that gene expression profiling in the mice model would extend our understanding of atherosclerosis in the molecular level. This study provides a fundamental framework for future clinical research on human atherosclerosis and new clues for developing novel drugs for the treatment of atherosclerosis.
Insights
AMP-activated protein kinase (AMPK) activators IMM-H007, Metformin, and A-769662 were tested in an atherosclerosis mouse model. Metformin and IMM-H007 showed similar therapeutic effects, impacting seven key pathways.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pharmacology
Background:
- Atherosclerosis, a primary cause of cardiovascular diseases, involves lipid deposition driven by suppressed AMP-activated protein kinase (AMPK).
- Understanding AMPK's role is crucial for developing effective atherosclerosis treatments.
Purpose of the Study:
- To develop a mouse model of atherosclerosis and evaluate the therapeutic efficacy of three AMPK activators: IMM-H007, A-769662, and Metformin.
- To identify the superior AMPK activator for treating atherosclerosis based on gene expression profiling.
Main Methods:
- Developed a mouse model for atherosclerosis.
- Administered three AMPK activators (IMM-H007, A-769662, Metformin) to assess therapeutic effects.
- Analyzed liver transcriptomes of high-fat diet and treatment groups to identify differentially expressed genes and metabolic pathways.
Main Results:
- A total of 799 differentially expressed genes were identified across the treatment groups compared to the high-fat diet group.
- IMM-H007, Metformin, and A-769662 affected 291, 473, and 323 genes, respectively.
- Seven statistically significant metabolic and disease pathways were commonly affected by both IMM-H007 and Metformin treatments.
Conclusions:
- Gene expression profiling in this mouse model enhances molecular understanding of atherosclerosis.
- The study provides a framework for human atherosclerosis research and identifies potential drug development leads.
- IMM-H007 and Metformin demonstrate comparable therapeutic potential in the atherosclerosis model.
