首都医科大学学报 ›› 2025, Vol. 46 ›› Issue (5): 924-933.doi: 10.3969/j.issn.1006-7795.2025.05.024

• 综述 • 上一篇    下一篇

动脉粥样硬化小鼠模型研究进展

马  薇1  姜慧敏1  周一帆1  张炜月2  李  慧3  周  陈1 *#  吉训明1,3 *#   

  1. 1.首都医科大学脑重大疾病研究中心,北京 100069; 2. 北京航空航天大学生物与医学工程学院大数据精准医疗高精尖中心,北京 100191; 3.首都医科大学宣武医院神经外科,北京 100053
  • 收稿日期:2025-04-14 修回日期:2025-05-12 出版日期:2025-10-21 发布日期:2025-10-22
  • 通讯作者: 周 陈, ​ 吉训明 E-mail:chenzhou2013abc@163.com; jixm@ccmu.edu.com

Research progress in mouse model of atherosclerosis

Ma Wei 1,Jiang Huimin 1,Zhou Yifan 1,Zhang Weiyue 2,Li Hui 3,Zhou Chen1*# , Ji Xunming1,3 *#   

  1. 1.Center for Brain Disorders, Capital Medical University, Beijing 100069, China; 2. Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, School of Biological Science and Medical Engineering, Beihang University, Beijing 100191, China; 3. Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, China
  • Received:2025-04-14 Revised:2025-05-12 Online:2025-10-21 Published:2025-10-22

摘要: 心血管疾病是全球范围内造成死亡的最主要原因,其核心病理改变动脉粥样硬化(atherosclerosis,AS)是一种多因素驱动的慢性炎症性疾病。AS发病机制涉及脂代谢紊乱、炎症反应与斑块易损性等多重病理环节,其复杂性要求动物模型需精准模拟特定病理特征。基因工程小鼠凭借遗传背景可编辑性、表型可追踪性及与人类病理的分子保守性,成为解析AS机制的核心工具。本文将对主要AS小鼠模型构建方法进行概述,重点分析饮食诱导、遗传修饰及物理损伤等不同的建模方法在模拟病理特征和表型稳定性方面的效果。 

关键词: 心血管病, 动脉粥样硬化, 动物模型, 载脂蛋白E, 低密度脂蛋白受体, 斑块

Abstract: Cardiovascular disease is the leading cause of death worldwide, with atherosclerosis (AS)-its core pathological manifestation-representing a multifactorial-driven chronic inflammatory disorder. The pathogenesis of AS involves intricate pathological mechanisms including dyslipidemia, inflammatory cascades, and plaque vulnerability, whose complexity necessitates animal models capable of accurately recapitulating specific pathological features. Genetically engineered murine models have emerged as pivotal tools for deciphering AS mechanisms, owing to their genetic manipulability, phenotypic traceability, and molecular conservation with human pathophysiology. This review provides a systematic overview of current methodologies for establishing AS mouse models, with particular emphasis on evaluating the pathological fidelity of dietary induction approaches, genetic modification strategies [notably apolipoprotein E (ApoE)-/- and low density lipoproteins receptor (LDLr)-/- models], and physical injury paradigms.

Key words: cardiovascular disease, atherosclerosis, animal models, apolipoprotein E (ApoE), low density lipoproteins receptor (LDLr), plaque

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