Mouse Models of Aortic Pathologies: Deciphering Molecular and Cellular Mechanisms from Bench to Bedside

IF 2.1 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
CJC Open Pub Date : 2026-10-01 Epub Date: 2026-06-29 DOI:10.1016/j.cjco.2026.06.010
Alicia Baptista Vicente PhD, Alexis Richard PhD, Clara Gourhand MSc, Céline Fassot PhD, Laurent Loufrani PhD
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引用次数: 0

Abstract

Background

Aortic pathologies, including abdominal aortic aneurysm, thoracic aortic aneurysm, and aortic dissection, are life-threatening conditions characterized by complex pathophysiology and a lack of simple, early, and reliable diagnostic tools.

Methods

This review synthesizes current knowledge on the molecular and cellular mechanisms underlying aortic pathologies, with a particular focus on vascular smooth muscle cell dysfunction, extracellular matrix degradation, and inflammatory signaling pathways. The review critically evaluates the strengths and limitations of widely used murine models, including elastase infusion, calcium chloride application, angiotensin II infusion, and β-aminopropionitrile administration, in the context of current clinical knowledge.

Results

Murine models provide valuable insights into the early stages of disease, which are often inaccessible in humans, and have been instrumental in elucidating key mechanisms involved in aneurysm formation and dissection. These models differ in their anatomic specificity, vascular remodelling dynamics, immune activation profiles, and translational relevance. Emerging complementary approaches, including advanced translational platforms and computational models, further improve the interpretation and translational value of preclinical findings.

Conclusions

By linking experimental findings to clinical perspectives, this review proposes a bench-to-bedside framework for the study of aortic disease. Integrating complementary experimental models with human-relevant systems may improve mechanistic understanding and support future diagnostic and therapeutic strategies innovation in aortic aneurysm and dissection.
主动脉病变小鼠模型:从实验室到床边解读分子和细胞机制
主动脉病变,包括腹主动脉瘤、胸主动脉瘤和主动脉夹层,是危及生命的疾病,其特点是病理生理复杂,缺乏简单、早期和可靠的诊断工具。本文综述了主动脉病变的分子和细胞机制,特别关注血管平滑肌细胞功能障碍、细胞外基质降解和炎症信号通路。在当前的临床知识背景下,该综述批判性地评估了广泛使用的小鼠模型的优势和局限性,包括弹性蛋白酶输注、氯化钙应用、血管紧张素II输注和β-氨基丙腈给药。结果尿液模型为疾病的早期阶段提供了有价值的见解,这在人类中通常是无法获得的,并且有助于阐明动脉瘤形成和夹层的关键机制。这些模型在解剖特异性、血管重塑动力学、免疫激活概况和翻译相关性方面有所不同。新兴的互补方法,包括先进的转化平台和计算模型,进一步提高了临床前研究结果的解释和转化价值。通过将实验结果与临床观点联系起来,本综述提出了一个从实验室到床边的主动脉疾病研究框架。将互补的实验模型与人类相关的系统相结合,可以提高对主动脉瘤和夹层的机制理解,并支持未来诊断和治疗策略的创新。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CJC Open
CJC Open Medicine-Cardiology and Cardiovascular Medicine
CiteScore
3.30
自引率
0.00%
发文量
143
审稿时长
60 days
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