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Related Experiment Video

Updated: Feb 4, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
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Apolipoprotein E deficiency accelerates atherosclerosis development in miniature pigs.

Bin Fang1, Xueyang Ren1, Ying Wang1,2

  • 1Jiangsu Key Laboratory of Xenotransplantation, Nanjing Medical University, Nanjing 211166, China.

Disease Models & Mechanisms
|October 12, 2018
PubMed
Summary

Genetically engineered miniature pigs lacking Apolipoprotein E (ApoE) offer a valuable model for atherosclerosis research. These pigs develop human-like cardiovascular disease, aiding translational studies.

Keywords:
ApoEAtherosclerosisBama miniature pigsCRISPR/Cas9

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Area of Science:

  • Cardiovascular Science
  • Genetics
  • Animal Models

Background:

  • Miniature pigs share physiological similarities with humans, making them suitable for cardiovascular disease modeling.
  • Apolipoprotein E (ApoE) deficiency is a known factor in human cardiovascular disease, particularly familial hypercholesterolemia and atherosclerosis.
  • Existing animal models may not fully replicate the complexity of human atherosclerosis.

Purpose of the Study:

  • To develop an improved large animal model for familial hypercholesterolemia and atherosclerosis.
  • To utilize CRISPR/Cas9 gene editing technology to create ApoE-deficient miniature pigs.

Main Methods:

  • The clustered regularly interspaced short palindromic repeats (CRISPR)-associated protein 9 system (CRISPR/Cas9) was employed to disrupt the Apolipoprotein E (ApoE) gene in Bama miniature pigs.
  • Biallelic-modified pigs with both in-frame and frameshift mutations in the ApoE gene were generated.
  • The pigs were fed either a regular chow diet or a high-fat, high-cholesterol (HFHC) diet for six months.

Main Results:

  • ApoE-deficient pigs showed moderately elevated plasma cholesterol on a standard diet.
  • After six months on an HFHC diet, these pigs developed severe hypercholesterolemia.
  • Spontaneous development of atherosclerotic lesions, resembling those in humans, was observed in the aorta and coronary arteries of the ApoE-deficient pigs.

Conclusions:

  • The generated ApoE-deficient miniature pigs serve as a valuable large animal model for studying atherosclerosis.
  • This model holds promise for advancing translational research in cardiovascular disease, particularly for understanding familial hypercholesterolemia and atherosclerosis.
  • The model's human-like pathology facilitates deeper insights into disease mechanisms and potential therapeutic strategies.