Large animal models of cardiovascular disease

被引:99
|
作者
Tsang, H. G. [1 ]
Rashdan, N. A. [1 ]
Whitelaw, C. B. A. [1 ]
Corcoran, B. M. [2 ]
Summers, K. M. [1 ]
MacRae, V. E. [1 ]
机构
[1] Univ Edinburgh, Roslin Inst, Royal Dick Sch Vet Studies, Easter Bush EH25 9RG, Midlothian, Scotland
[2] Univ Edinburgh, Royal Dick Sch Vet Studies, Easter Bush EH25 9RG, Midlothian, Scotland
基金
英国生物技术与生命科学研究理事会;
关键词
cardiovascular disease; large animal models; calcific aortic valve disease; aortic stenosis; vascular calcification; Marfan syndrome; genetic engineering; LOW-DENSITY-LIPOPROTEIN; AORTIC-VALVE DISEASE; VALVULAR ENDOTHELIAL-CELLS; SMOOTH-MUSCLE-CELLS; GENERALIZED ARTERIAL CALCIFICATION; INTIMA-MEDIA THICKNESS; COMPLEX ATHEROSCLEROTIC LESIONS; CORONARY-HEART-DISEASE; CHRONIC-RENAL-FAILURE; MATRIX GLA-PROTEIN;
D O I
10.1002/cbf.3173
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The human cardiovascular system is a complex arrangement of specialized structures with distinct functions. The molecular landscape, including the genome, transcriptome and proteome, is pivotal to the biological complexity of both normal and abnormal mammalian processes. Despite our advancing knowledge and understanding of cardiovascular disease (CVD) through the principal use of rodent models, this continues to be an increasing issue in today's world. For instance, as the ageing population increases, so does the incidence of heart valve dysfunction. This may be because of changes in molecular composition and structure of the extracellular matrix, or from the pathological process of vascular calcification in which bone-formation related factors cause ectopic mineralization. However, significant differences between mice and men exist in terms of cardiovascular anatomy, physiology and pathology. In contrast, large animal models can show considerably greater similarity to humans. Furthermore, precise and efficient genome editing techniques enable the generation of tailored models for translational research. These novel systems provide a huge potential for large animal models to investigate the regulatory factors and molecular pathways that contribute to CVD in vivo. In turn, this will help bridge the gap between basic science and clinical applications by facilitating the refinement of therapies for cardiovascular disease. Copyright (c) 2016 John Wiley & Sons, Ltd.
引用
收藏
页码:113 / 132
页数:20
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