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Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
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Related Experiment Video

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A severe atherosclerosis mouse model on the resistant NOD background.

Xugang Wang1,2, Rong Huang1,2, Lichen Zhang1,2

  • 1Laboratory of Genetic Regulators in the Immune System, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Henan Province 453003, China.

Disease Models & Mechanisms
|October 12, 2018
PubMed
Summary

Researchers developed a new mouse model for atherosclerosis by genetically modifying Non-obese diabetic (NOD) mice. This model exhibits severe atherosclerosis and autoimmune traits, aiding research into cardiovascular disease in diabetic and autoimmune conditions.

Keywords:
ApoEAtherosclerosisCRISPR/Cas9LDLRNOD

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Genetics

Background:

  • Atherosclerosis is a complex arterial disease with life-threatening consequences.
  • Existing atherosclerosis models do not fully represent human disease on diabetic and autoimmune backgrounds.
  • Non-obese diabetic (NOD) mice are valuable for studying autoimmunity and diabetes.

Purpose of the Study:

  • To develop a novel genetic atherosclerosis model on the NOD mouse background.
  • To investigate atherosclerosis development in genetically modified NOD mice with disrupted apolipoprotein E (ApoE) and low-density lipoprotein receptor (LDLR) genes.
  • To compare the phenotype of these novel NOD models with standard ApoE-deficient C57BL/6 mice.

Main Methods:

  • CRISPR/Cas9 genome editing was used to create NOD mice with targeted ApoE and LDLR gene disruptions.
  • Single and double knockout NOD mice were generated and compared.
  • Mice were fed a high-fat diet (HFD) to induce hyperlipidemia and assess atherosclerosis severity and immune response.

Main Results:

  • Single ApoE or LDLR gene disruption in NOD mice did not induce significant atherosclerosis.
  • Double knockout NOD mice (ApoE/LDLR deficient) fed a HFD developed severe atherosclerosis, with aortic plaque narrowing exceeding 60%.
  • These double knockout NOD mice also exhibited pancreatic islet destruction and an inflammatory response to hyperlipidemia.

Conclusions:

  • A novel genetic model of severe atherosclerosis on the NOD background has been successfully created.
  • This model recapitulates key features of atherosclerosis in the context of autoimmunity and diabetes.
  • The double knockout NOD mouse is a valuable tool for studying atherosclerosis in individuals with underlying autoimmune conditions.