Cargando…
Large animal models of cardiovascular disease
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 knowle...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2016
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4834612/ https://www.ncbi.nlm.nih.gov/pubmed/26914991 http://dx.doi.org/10.1002/cbf.3173 |
_version_ | 1782427514881179648 |
---|---|
author | Tsang, H. G. Rashdan, N. A. Whitelaw, C. B. A. Corcoran, B. M. Summers, K. M. MacRae, V. E. |
author_facet | Tsang, H. G. Rashdan, N. A. Whitelaw, C. B. A. Corcoran, B. M. Summers, K. M. MacRae, V. E. |
author_sort | Tsang, H. G. |
collection | PubMed |
description | 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. 2016 The Authors. Published by John Wiley & Sons Ltd. |
format | Online Article Text |
id | pubmed-4834612 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-48346122016-05-05 Large animal models of cardiovascular disease Tsang, H. G. Rashdan, N. A. Whitelaw, C. B. A. Corcoran, B. M. Summers, K. M. MacRae, V. E. Cell Biochem Funct Review Article 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. 2016 The Authors. Published by John Wiley & Sons Ltd. John Wiley and Sons Inc. 2016-02-24 2016-04 /pmc/articles/PMC4834612/ /pubmed/26914991 http://dx.doi.org/10.1002/cbf.3173 Text en 2016 The Authors. Published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Tsang, H. G. Rashdan, N. A. Whitelaw, C. B. A. Corcoran, B. M. Summers, K. M. MacRae, V. E. Large animal models of cardiovascular disease |
title | Large animal models of cardiovascular disease |
title_full | Large animal models of cardiovascular disease |
title_fullStr | Large animal models of cardiovascular disease |
title_full_unstemmed | Large animal models of cardiovascular disease |
title_short | Large animal models of cardiovascular disease |
title_sort | large animal models of cardiovascular disease |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4834612/ https://www.ncbi.nlm.nih.gov/pubmed/26914991 http://dx.doi.org/10.1002/cbf.3173 |
work_keys_str_mv | AT tsanghg largeanimalmodelsofcardiovasculardisease AT rashdanna largeanimalmodelsofcardiovasculardisease AT whitelawcba largeanimalmodelsofcardiovasculardisease AT corcoranbm largeanimalmodelsofcardiovasculardisease AT summerskm largeanimalmodelsofcardiovasculardisease AT macraeve largeanimalmodelsofcardiovasculardisease |