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高胆固醇血症小鼠动脉粥样硬化量化的综述

A mini-review on quantification of atherosclerosis in hypercholesterolemic mice.

作者信息

Chen Hui, Howatt Deborah A, Franklin Michael K, Amioka Naofumi, Sawada Hisashi, Daugherty Alan, Lu Hong S

机构信息

Saha Cardiovascular Research Center, University of Kentucky, Lexington, Kentucky, United States.

Saha Aortic Center, University of Kentucky, Lexington, Kentucky, United States.

出版信息

Glob Transl Med. 2022;1(1). doi: 10.36922/gtm.v1i1.76. Epub 2022 Jun 14.

DOI:10.36922/gtm.v1i1.76
PMID:35925518
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9345319/
Abstract

Atherosclerosis is a leading cause of morbidity and mortality in many countries. Mice are the most frequently used animal model to study the pathogenesis and molecular mechanisms of atherosclerosis. analyses of the aorta and cross-sections of the aortic root are the two common modes for quantifying the severity of atherosclerosis in mice. This mini-review introduces these two methods, discusses their pros and cons, and provides suggestions to optimize the quantification of atherosclerosis, thereby enhancing rigor and reproducibility in preclinical research.

摘要

动脉粥样硬化是许多国家发病和死亡的主要原因。小鼠是研究动脉粥样硬化发病机制和分子机制最常用的动物模型。对主动脉和主动脉根部横截面的分析是量化小鼠动脉粥样硬化严重程度的两种常见方式。本综述介绍这两种方法,讨论其优缺点,并提供优化动脉粥样硬化量化的建议,从而提高临床前研究的严谨性和可重复性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a21b/9345319/40ea53a2f124/nihms-1816986-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a21b/9345319/70d9488442d9/nihms-1816986-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a21b/9345319/40ea53a2f124/nihms-1816986-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a21b/9345319/70d9488442d9/nihms-1816986-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a21b/9345319/40ea53a2f124/nihms-1816986-f0002.jpg

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本文引用的文献

1
Updates on Approaches for Studying Atherosclerosis.动脉粥样硬化研究方法的最新进展。
Arterioscler Thromb Vasc Biol. 2019 Apr;39(4):e108-e117. doi: 10.1161/ATVBAHA.119.312001.
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Recommendation on Design, Execution, and Reporting of Animal Atherosclerosis Studies: A Scientific Statement From the American Heart Association.《动物动脉粥样硬化研究的设计、实施及报告建议:美国心脏协会科学声明》
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Hypercholesterolemia Induced by a PCSK9 Gain-of-Function Mutation Augments Angiotensin II-Induced Abdominal Aortic Aneurysms in C57BL/6 Mice-Brief Report.
肾近端小管细胞特异性巨蛋白缺失不影响动脉粥样硬化,但在喂食西方饮食的小鼠中诱发肾小管间质性肾炎。
Arterioscler Thromb Vasc Biol. 2025 Jan;45(1):74-89. doi: 10.1161/ATVBAHA.124.321366. Epub 2024 Nov 21.
4
Renal Proximal Tubule Cell-specific Megalin Deletion Does Not Affect Atherosclerosis But Induces Tubulointerstitial Nephritis in Mice Fed Western Diet.肾近端小管细胞特异性巨蛋白缺失不影响动脉粥样硬化,但在喂食西式饮食的小鼠中诱发肾小管间质性肾炎。
bioRxiv. 2024 Sep 27:2024.05.11.592234. doi: 10.1101/2024.05.11.592234.
5
Trehalose promotes atherosclerosis regression in female mice.海藻糖可促进雌性小鼠的动脉粥样硬化消退。
Front Cardiovasc Med. 2024 Feb 16;11:1298014. doi: 10.3389/fcvm.2024.1298014. eCollection 2024.
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Endothelial nitric oxide synthase (eNOS) S1176 phosphorylation status governs atherosclerotic lesion formation.内皮型一氧化氮合酶(eNOS)S1176位点的磷酸化状态决定动脉粥样硬化病变的形成。
Front Cardiovasc Med. 2023 Nov 14;10:1279868. doi: 10.3389/fcvm.2023.1279868. eCollection 2023.
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Front Cardiovasc Med. 2023 Aug 16;10:1250234. doi: 10.3389/fcvm.2023.1250234. eCollection 2023.
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Atherosclerosis. 2016 Aug;251:109-118. doi: 10.1016/j.atherosclerosis.2016.06.011. Epub 2016 Jun 9.
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Arterioscler Thromb Vasc Biol. 2015 Jan;35(1):11-2. doi: 10.1161/ATVBAHA.114.304833.
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Arterioscler Thromb Vasc Biol. 2015 Jan;35(1):50-9. doi: 10.1161/ATVBAHA.114.303617. Epub 2014 Oct 23.
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AAV vectors expressing LDLR gain-of-function variants demonstrate increased efficacy in mouse models of familial hypercholesterolemia.AAV 载体表达 LDLR 获得性功能变异体在家族性高胆固醇血症的小鼠模型中显示出更高的疗效。
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Stabilisation of atherosclerotic plaques. Position paper of the European Society of Cardiology (ESC) Working Group on atherosclerosis and vascular biology.动脉粥样硬化斑块的稳定。欧洲心脏病学会(ESC)动脉粥样硬化和血管生物学工作组立场文件。
Thromb Haemost. 2011 Jul;106(1):1-19. doi: 10.1160/TH10-12-0784. Epub 2011 Jun 14.