TY - JOUR
T1 - Large animal models of cardiovascular disease
AU - Tsang, Hiu-Gwen
AU - Rashdan, Nabil
AU - Whitelaw, Christopher
AU - Corcoran, Brendan
AU - Summers, Kim
AU - MacRae, Victoria
PY - 2016/2/24
Y1 - 2016/2/24
N2 - The human cardiovascular system is a complex arrangement of specialised 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 aging population increases, so does the incidence of heart valve dysfunction. This may be due to 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 mineralisation. 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.
AB - The human cardiovascular system is a complex arrangement of specialised 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 aging population increases, so does the incidence of heart valve dysfunction. This may be due to 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 mineralisation. 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.
KW - Cardiovascular disease
KW - Calcific aortic valve disease
KW - Aortic stenosis
KW - Vascular calcification
KW - Marfan syndrome
KW - Genetic engineering
KW - Atherosclerosis
KW - Animal models
U2 - 10.1002/cbf.3173
DO - 10.1002/cbf.3173
M3 - Article
SN - 0263-6484
VL - 34
SP - 113
EP - 132
JO - Cell Biochemistry and Function
JF - Cell Biochemistry and Function
IS - 3
ER -