CD73 (Cluster of Differentiation 73) and the Differences Between Mice and Humans
CD73 (Cluster of Differentiation 73) and the Differences Between Mice and Humans
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DOI：
10.1161/atvbaha.118.311579
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发表时间：
2019-03-01
影响因子：
8.7
通讯作者：
St Hilaire, Cynthia
中科院分区：
文献类型：
--
作者：
Joolharzadeh, Pouya;St Hilaire, Cynthia
由于血管疾病是复杂的，各种表现受到不同血管床结构、剪切力和机械力、所涉及的细胞类型和炎症反应的影响，因此有必要建立体内模型来概括发病过程中复杂的生理和动态细胞相互作用。小鼠基因敲除模型是研究人员研究特定基因或途径在多方面疾病特征中的作用的常用工具。尽管有价值，但这些模型并不完美，对于CD73(分化簇73)来说尤其如此，CD73是一种从AMP产生腺苷的细胞外酶。在基线水平，CD73缺陷小鼠没有明显的表型，而CD73缺陷的人类则呈现血管钙化、动脉增大和弯曲以及小关节钙化的复杂表型。在这篇综述中，我们强调了老鼠和人类系统之间的差异，并讨论了利用老鼠的发现来告知我们人类状况的可能性。
As vascular disease is complex and the various manifestations are influenced by differences in vascular bed architecture, exposure to shear and mechanical forces, cell types involved, and inflammatory responses, in vivo models are necessary to recapitulate the complex physiology and dynamic cellular interactions during pathogenesis. Murine knockout models are commonly used tools for investigators to study the role of a specific gene or pathway in multifaceted disease traits. Although valuable, these models are not perfect, and this is particularly true in regard to CD73 (cluster of differentiation 73), the extracellular enzyme that generates adenosine from AMP. At baseline, CD73-deficient mice do not present with an overt phenotype, whereas CD73-deficient humans present with the complex phenotype of vascular calcification, arteriomegaly and tortuosity, and calcification in small joints. In this review, we highlight the differences between the mouse and human systems and discuss the potential to leverage findings in mice to inform us on the human conditions.