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Large animal models of cardiovascular disease.

Tsang HG, Rashdan NA, Whitelaw CB, Corcoran BM, Summers KM, MacRae VE - Cell Biochem. Funct. (2016)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: The Roslin Institute, Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian, SCT, UK.

No MeSH data available.


Related in: MedlinePlus

Simplified cross section of the aortic valve showing progression of aortic valve calcification. Valve endothelial cells (VECs) line the valve leaflet surface. The inner layers of the valve consist of the fibrosa, spongiosa and ventricularis. The principal cell type within each layer is the valve interstitial cells (VICs). The fibrosa contains collagen (Types I and III), the spongiosa contains glycosaminoglycans (GAGs) and the ventricularis—elastin fibres. In calcific aortic valve disease (CAVD), often the fibrosa layer becomes calcified and thickened. This may be because of lipid deposition and inflammatory processes which trigger the osteochondrogenic transdifferentiation of VICs. Calcium deposition then occurs, forming bone‐like material as neovascularization around the calcified lesions and remodelling of the extracellular matrix occurs. This results in the formation of calcified nodules and the thickening of the valve leaflet
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cbf3173-fig-0001: Simplified cross section of the aortic valve showing progression of aortic valve calcification. Valve endothelial cells (VECs) line the valve leaflet surface. The inner layers of the valve consist of the fibrosa, spongiosa and ventricularis. The principal cell type within each layer is the valve interstitial cells (VICs). The fibrosa contains collagen (Types I and III), the spongiosa contains glycosaminoglycans (GAGs) and the ventricularis—elastin fibres. In calcific aortic valve disease (CAVD), often the fibrosa layer becomes calcified and thickened. This may be because of lipid deposition and inflammatory processes which trigger the osteochondrogenic transdifferentiation of VICs. Calcium deposition then occurs, forming bone‐like material as neovascularization around the calcified lesions and remodelling of the extracellular matrix occurs. This results in the formation of calcified nodules and the thickening of the valve leaflet

Mentions: There are four cardiac valves: the mitral (bicuspid) valve and aortic semilunar valve on the left side of the heart, and the tricuspid valve and pulmonary semilunar valve on the right side. The heart valve leaflet structure consists of cellular and extracellular components. Extracellular components include collagen, glycosaminoglycans (GAGs) and elastin present in the three layers of the valve: the fibrosa, spongiosa and ventricularis, respectively (Figure 1) 19, 20, 21, 22. Valve surface endothelial cells (VECs) and the inner valve interstitial cells (VICs) are the principal cell types found in the cardiac valves 19, 20, 23.


Large animal models of cardiovascular disease.

Tsang HG, Rashdan NA, Whitelaw CB, Corcoran BM, Summers KM, MacRae VE - Cell Biochem. Funct. (2016)

Simplified cross section of the aortic valve showing progression of aortic valve calcification. Valve endothelial cells (VECs) line the valve leaflet surface. The inner layers of the valve consist of the fibrosa, spongiosa and ventricularis. The principal cell type within each layer is the valve interstitial cells (VICs). The fibrosa contains collagen (Types I and III), the spongiosa contains glycosaminoglycans (GAGs) and the ventricularis—elastin fibres. In calcific aortic valve disease (CAVD), often the fibrosa layer becomes calcified and thickened. This may be because of lipid deposition and inflammatory processes which trigger the osteochondrogenic transdifferentiation of VICs. Calcium deposition then occurs, forming bone‐like material as neovascularization around the calcified lesions and remodelling of the extracellular matrix occurs. This results in the formation of calcified nodules and the thickening of the valve leaflet
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4834612&req=5

cbf3173-fig-0001: Simplified cross section of the aortic valve showing progression of aortic valve calcification. Valve endothelial cells (VECs) line the valve leaflet surface. The inner layers of the valve consist of the fibrosa, spongiosa and ventricularis. The principal cell type within each layer is the valve interstitial cells (VICs). The fibrosa contains collagen (Types I and III), the spongiosa contains glycosaminoglycans (GAGs) and the ventricularis—elastin fibres. In calcific aortic valve disease (CAVD), often the fibrosa layer becomes calcified and thickened. This may be because of lipid deposition and inflammatory processes which trigger the osteochondrogenic transdifferentiation of VICs. Calcium deposition then occurs, forming bone‐like material as neovascularization around the calcified lesions and remodelling of the extracellular matrix occurs. This results in the formation of calcified nodules and the thickening of the valve leaflet
Mentions: There are four cardiac valves: the mitral (bicuspid) valve and aortic semilunar valve on the left side of the heart, and the tricuspid valve and pulmonary semilunar valve on the right side. The heart valve leaflet structure consists of cellular and extracellular components. Extracellular components include collagen, glycosaminoglycans (GAGs) and elastin present in the three layers of the valve: the fibrosa, spongiosa and ventricularis, respectively (Figure 1) 19, 20, 21, 22. Valve surface endothelial cells (VECs) and the inner valve interstitial cells (VICs) are the principal cell types found in the cardiac valves 19, 20, 23.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: The Roslin Institute, Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian, SCT, UK.

No MeSH data available.


Related in: MedlinePlus