Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis
Abstract Pathologic cardiac hypertrophy is a common consequence of many cardiovascular diseases, including aortic stenosis (AS). AS is known to increase the pressure load of the left ventricle, causing a compensative response of the cardiac muscle, which progressively will lead to dilation and heart...
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Oxford University Press (OUP)
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croxfordunivpr:10.1093/cvr/cvae045 2024-05-19T07:38:44+00:00 Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis Beslika, Evangelia Leite-Moreira, Adelino De Windt, Leon J da Costa Martins, Paula A 2024 http://dx.doi.org/10.1093/cvr/cvae045 https://academic.oup.com/cardiovascres/advance-article-pdf/doi/10.1093/cvr/cvae045/56817320/cvae045.pdf https://academic.oup.com/cardiovascres/article-pdf/120/5/461/57362169/cvae045.pdf en eng Oxford University Press (OUP) https://creativecommons.org/licenses/by-nc/4.0/ Cardiovascular Research volume 120, issue 5, page 461-475 ISSN 0008-6363 1755-3245 journal-article 2024 croxfordunivpr https://doi.org/10.1093/cvr/cvae045 2024-05-02T09:31:32Z Abstract Pathologic cardiac hypertrophy is a common consequence of many cardiovascular diseases, including aortic stenosis (AS). AS is known to increase the pressure load of the left ventricle, causing a compensative response of the cardiac muscle, which progressively will lead to dilation and heart failure. At a cellular level, this corresponds to a considerable increase in the size of cardiomyocytes, known as cardiomyocyte hypertrophy, while their proliferation capacity is attenuated upon the first developmental stages. Cardiomyocytes, in order to cope with the increased workload (overload), suffer alterations in their morphology, nuclear content, energy metabolism, intracellular homeostatic mechanisms, contractile activity, and cell death mechanisms. Moreover, modifications in the cardiomyocyte niche, involving inflammation, immune infiltration, fibrosis, and angiogenesis, contribute to the subsequent events of a pathologic hypertrophic response. Considering the emerging need for a better understanding of the condition and treatment improvement, as the only available treatment option of AS consists of surgical interventions at a late stage of the disease, when the cardiac muscle state is irreversible, large animal models have been developed to mimic the human condition, to the greatest extend. Smaller animal models lack physiological, cellular and molecular mechanisms that sufficiently resemblance humans and in vitro techniques yet fail to provide adequate complexity. Animals, such as the ferret (Mustello purtorius furo), lapine (rabbit, Oryctolagus cunigulus), feline (cat, Felis catus), canine (dog, Canis lupus familiaris), ovine (sheep, Ovis aries), and porcine (pig, Sus scrofa), have contributed to research by elucidating implicated cellular and molecular mechanisms of the condition. Essential discoveries of each model are reported and discussed briefly in this review. Results of large animal experimentation could further be interpreted aiming at prevention of the disease progress or, alternatively, at ... Article in Journal/Newspaper Canis lupus Oxford University Press Cardiovascular Research |
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Oxford University Press |
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English |
description |
Abstract Pathologic cardiac hypertrophy is a common consequence of many cardiovascular diseases, including aortic stenosis (AS). AS is known to increase the pressure load of the left ventricle, causing a compensative response of the cardiac muscle, which progressively will lead to dilation and heart failure. At a cellular level, this corresponds to a considerable increase in the size of cardiomyocytes, known as cardiomyocyte hypertrophy, while their proliferation capacity is attenuated upon the first developmental stages. Cardiomyocytes, in order to cope with the increased workload (overload), suffer alterations in their morphology, nuclear content, energy metabolism, intracellular homeostatic mechanisms, contractile activity, and cell death mechanisms. Moreover, modifications in the cardiomyocyte niche, involving inflammation, immune infiltration, fibrosis, and angiogenesis, contribute to the subsequent events of a pathologic hypertrophic response. Considering the emerging need for a better understanding of the condition and treatment improvement, as the only available treatment option of AS consists of surgical interventions at a late stage of the disease, when the cardiac muscle state is irreversible, large animal models have been developed to mimic the human condition, to the greatest extend. Smaller animal models lack physiological, cellular and molecular mechanisms that sufficiently resemblance humans and in vitro techniques yet fail to provide adequate complexity. Animals, such as the ferret (Mustello purtorius furo), lapine (rabbit, Oryctolagus cunigulus), feline (cat, Felis catus), canine (dog, Canis lupus familiaris), ovine (sheep, Ovis aries), and porcine (pig, Sus scrofa), have contributed to research by elucidating implicated cellular and molecular mechanisms of the condition. Essential discoveries of each model are reported and discussed briefly in this review. Results of large animal experimentation could further be interpreted aiming at prevention of the disease progress or, alternatively, at ... |
format |
Article in Journal/Newspaper |
author |
Beslika, Evangelia Leite-Moreira, Adelino De Windt, Leon J da Costa Martins, Paula A |
spellingShingle |
Beslika, Evangelia Leite-Moreira, Adelino De Windt, Leon J da Costa Martins, Paula A Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis |
author_facet |
Beslika, Evangelia Leite-Moreira, Adelino De Windt, Leon J da Costa Martins, Paula A |
author_sort |
Beslika, Evangelia |
title |
Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis |
title_short |
Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis |
title_full |
Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis |
title_fullStr |
Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis |
title_full_unstemmed |
Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis |
title_sort |
large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis |
publisher |
Oxford University Press (OUP) |
publishDate |
2024 |
url |
http://dx.doi.org/10.1093/cvr/cvae045 https://academic.oup.com/cardiovascres/advance-article-pdf/doi/10.1093/cvr/cvae045/56817320/cvae045.pdf https://academic.oup.com/cardiovascres/article-pdf/120/5/461/57362169/cvae045.pdf |
genre |
Canis lupus |
genre_facet |
Canis lupus |
op_source |
Cardiovascular Research volume 120, issue 5, page 461-475 ISSN 0008-6363 1755-3245 |
op_rights |
https://creativecommons.org/licenses/by-nc/4.0/ |
op_doi |
https://doi.org/10.1093/cvr/cvae045 |
container_title |
Cardiovascular Research |
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