4.4 Review

Large animal models of cardiovascular disease

期刊

CELL BIOCHEMISTRY AND FUNCTION
卷 34, 期 3, 页码 113-132

出版社

WILEY
DOI: 10.1002/cbf.3173

关键词

cardiovascular disease; large animal models; calcific aortic valve disease; aortic stenosis; vascular calcification; Marfan syndrome; genetic engineering

资金

  1. Biotechnology and Biological Sciences Research Council (BBSRC) [BB/J004316/1, BB/F023928/1, BB/J01446X/1]
  2. BBSRC [BB/F023928/1, BBS/E/D/20211553, BBS/E/R/00001608, BBS/E/D/20221658, BBS/E/D/20221657] Funding Source: UKRI
  3. Biotechnology and Biological Sciences Research Council [BBS/E/D/20221657, BBS/E/D/20211553, BB/F023928/1, 1358668, BBS/E/R/00001608, BBS/E/D/20221658] Funding Source: researchfish

向作者/读者索取更多资源

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.

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