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<p>Atherosclerosis is a chronic, progressive arterial disease characterized by the deposition of lipids on the inner arterial walls, leading to plaque formation and serious cardiovascular events. Traditional mouse models of atherosclerosis require prolonged dietary induction to exhibit arterial lesions due to significant differences in lipid metabolism compared to humans. In contrast, Golden hamsters share a lipid metabolic profile more closely aligned with humans. In this study, we utilized CRISPR/Cas9 to generate ApoE knockout (ApoE<sup>−/−</sup>) hamsters using, which spontaneously developed atherosclerotic lesions in the arterial wall after 8 weeks on a standard chow diet. When fed on a high-cholesterol/high-fat diet, they exhibited even more severe aortic atherosclerosis, fatty liver, and liver fibrosis. Our findings demonstrated that the ApoE<sup>−/−</sup> hamster model is highly valuable tool for translational research, offering significant potential for studying hyperlipidemia and atherosclerosis in a context more relevant to human physiology.</p> Graphical Abstract <p></p>

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The ApoE-Null Golden Hamster: A Novel Model of Atherosclerosis

  • 期刊论文

  • 发表日期：

    2026年7月29日

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  • Guangming Fang,
  • Shiyue Zheng,
  • Jinxin Miao,
  • Yi Zeng,
  • Ying Peng,
  • Yafei Zhai,
  • Haoran Guo,
  • Jianyao Wang,
  • Yiming Dong,
  • Xiaoxu Tian,
  • Mengduan Liu,
  • Yangyang Liu,
  • Xiaowei Li,
  • Mengyu Wang,
  • Xiaoyan Zhao,
  • Jie Du,
  • Yaohe Wang,
  • Jianzeng Dong

摘要

Atherosclerosis is a chronic, progressive arterial disease characterized by the deposition of lipids on the inner arterial walls, leading to plaque formation and serious cardiovascular events. Traditional mouse models of atherosclerosis require prolonged dietary induction to exhibit arterial lesions due to significant differences in lipid metabolism compared to humans. In contrast, Golden hamsters share a lipid metabolic profile more closely aligned with humans. In this study, we utilized CRISPR/Cas9 to generate ApoE knockout (ApoE−/−) hamsters using, which spontaneously developed atherosclerotic lesions in the arterial wall after 8 weeks on a standard chow diet. When fed on a high-cholesterol/high-fat diet, they exhibited even more severe aortic atherosclerosis, fatty liver, and liver fibrosis. Our findings demonstrated that the ApoE−/− hamster model is highly valuable tool for translational research, offering significant potential for studying hyperlipidemia and atherosclerosis in a context more relevant to human physiology.

Graphical Abstract