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本文引用的文献

1
Separate origin of the main components of the left coronary artery in Syrian hamsters (Mesocricetus auratus).叙利亚仓鼠(金仓鼠)左冠状动脉主要分支的独立起源
J Vet Med A Physiol Pathol Clin Med. 2007 Aug;54(6):297-301. doi: 10.1111/j.1439-0442.2007.00928.x.
2
Myocardial infarct size measurement in the mouse chronic infarction model: comparison of area- and length-based approaches.小鼠慢性梗死模型中心肌梗死面积的测量:基于面积和长度方法的比较。
J Appl Physiol (1985). 2007 Jun;102(6):2104-11. doi: 10.1152/japplphysiol.00033.2007. Epub 2007 Mar 8.
3
Patterning of coronary arteries in wildtype and connexin43 knockout mice.野生型和连接蛋白43基因敲除小鼠冠状动脉的形态形成
Dev Dyn. 2006 Oct;235(10):2786-94. doi: 10.1002/dvdy.20887.
4
Distinct cardiac malformations caused by absence of connexin 43 in the neural crest and in the non-crest neural tube.神经嵴和非嵴神经管中连接蛋白43缺失导致的不同心脏畸形。
Development. 2006 May;133(10):2063-73. doi: 10.1242/dev.02374. Epub 2006 Apr 19.
5
Coronary artery embryogenesis in cardiac defects induced by retinoic acid in mice.维甲酸诱导的小鼠心脏缺陷中的冠状动脉胚胎发生
Birth Defects Res A Clin Mol Teratol. 2005 Dec;73(12):966-79. doi: 10.1002/bdra.20200.
6
Solitary coronary ostium in the aorta in Syrian hamsters. A morphological study of 130 cases.叙利亚仓鼠主动脉中孤立性冠状动脉口。130例形态学研究。
Cardiovasc Pathol. 2005 Nov-Dec;14(6):303-11. doi: 10.1016/j.carpath.2005.07.001.
7
Connexin43 deficiency causes dysregulation of coronary vasculogenesis.连接蛋白43缺乏会导致冠状动脉血管生成失调。
Dev Biol. 2005 Aug 15;284(2):479-98. doi: 10.1016/j.ydbio.2005.06.004.
8
A novel model of cryoinjury-induced myocardial infarction in the mouse: a comparison with coronary artery ligation.小鼠冷冻损伤诱导心肌梗死的新模型:与冠状动脉结扎模型的比较。
Am J Physiol Heart Circ Physiol. 2005 Sep;289(3):H1291-300. doi: 10.1152/ajpheart.00111.2005. Epub 2005 Apr 29.
9
Distinct mouse coronary anatomy and myocardial infarction consequent to ligation.小鼠独特的冠状动脉解剖结构以及结扎导致的心肌梗死。
Coron Artery Dis. 2005 Feb;16(1):41-4. doi: 10.1097/00019501-200502000-00008.
10
Myocardial infarction in the C57BL/6J mouse: a quantifiable and highly reproducible experimental model.C57BL/6J小鼠的心肌梗死:一种可量化且高度可重复的实验模型。
Cardiovasc Pathol. 2004 Mar-Apr;13(2):91-7. doi: 10.1016/S1054-8807(03)00129-7.

C57BL/6小鼠品系的冠状动脉:与突变模型比较的意义。

The coronary arteries of the C57BL/6 mouse strains: implications for comparison with mutant models.

作者信息

Fernández B, Durán A C, Fernández M C, Fernández-Gallego T, Icardo J M, Sans-Coma V

机构信息

Department of Animal Biology, University of Málaga, Málaga, Spain.

出版信息

J Anat. 2008 Jan;212(1):12-8. doi: 10.1111/j.1469-7580.2007.00838.x. Epub 2007 Dec 4.

DOI:10.1111/j.1469-7580.2007.00838.x
PMID:18067545
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2423383/
Abstract

There are few detailed descriptions of the coronary arterial patterns in the mouse. Some recent reports on coronary anomalies in mutant mouse models have uncovered the importance of several genes (i.e. iv and connexin43) in coronary morphogenesis. These mutations spontaneously appeared (iv) or were generated (connexin43) in a C57BL/6 background, which is widely used for the development of mutant mice. We have studied the origin and course of the main coronary arteries of two C57BL/6 mouse strains. Unusual anatomical coronary arterial patterns were found, including: solitary ostium in aorta, accessory ostium, high take-off, aortic intramural course, slit-like ostium, sinus-like ostium and origin of a septal artery from the left coronary artery. In humans, some of these conditions are clinically relevant. Most of these patterns, which differ from those observed in wild mice and Swiss albino mice, coincide with those previously found in iv/iv and connexin43 knockout mice. The results indicate that there is variability in the coronary arterial arrangement of the laboratory mouse. Care should be taken when analysing coronary phenotypes of mutant mouse models.

摘要

关于小鼠冠状动脉模式的详细描述很少。最近一些关于突变小鼠模型中冠状动脉异常的报告揭示了几个基因(即iv和连接蛋白43)在冠状动脉形态发生中的重要性。这些突变在广泛用于突变小鼠发育的C57BL/6背景中自发出现(iv)或被产生(连接蛋白43)。我们研究了两种C57BL/6小鼠品系主要冠状动脉的起源和走行。发现了不寻常的解剖学冠状动脉模式,包括:主动脉单一开口、副开口、高位起始、主动脉壁内走行、裂隙样开口、窦样开口以及间隔动脉起源于左冠状动脉。在人类中,其中一些情况具有临床相关性。这些模式中的大多数与在野生小鼠和瑞士白化小鼠中观察到的不同,与先前在iv/iv和连接蛋白43基因敲除小鼠中发现的一致。结果表明实验室小鼠的冠状动脉排列存在变异性。在分析突变小鼠模型的冠状动脉表型时应谨慎。