Research progress in mouse model of atherosclerosis

doi:10.3969/j.issn.1006-7795.2025.05.024

Abstract

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

CLC Number:

R543

Ma Wei , Jiang Huimin , Zhou Yifan , Zhang Weiyue , Li Hui , Zhou Chen , Ji Xunming. Research progress in mouse model of atherosclerosis[J]. Journal of Capital Medical University, 2025, 46(5): 924-933.

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