Version 1
: Received: 26 June 2024 / Approved: 26 June 2024 / Online: 26 June 2024 (14:19:03 CEST)
How to cite:
Risato, G.; Brañas Casas, R.; Cason, M.; Bueno Marinas, M.; Pinci, S.; De Gaspari, M.; Visentin, S.; Rizzo, S.; Thiene, G.; Basso, C.; Pilichou, K.; Tiso, N.; Celeghin, R. In Vivo Approaches to Understand Arrhythmogenic Cardiomyopathy: Perspectives on Animal Models. Preprints2024, 2024061854. https://doi.org/10.20944/preprints202406.1854.v1
Risato, G.; Brañas Casas, R.; Cason, M.; Bueno Marinas, M.; Pinci, S.; De Gaspari, M.; Visentin, S.; Rizzo, S.; Thiene, G.; Basso, C.; Pilichou, K.; Tiso, N.; Celeghin, R. In Vivo Approaches to Understand Arrhythmogenic Cardiomyopathy: Perspectives on Animal Models. Preprints 2024, 2024061854. https://doi.org/10.20944/preprints202406.1854.v1
Risato, G.; Brañas Casas, R.; Cason, M.; Bueno Marinas, M.; Pinci, S.; De Gaspari, M.; Visentin, S.; Rizzo, S.; Thiene, G.; Basso, C.; Pilichou, K.; Tiso, N.; Celeghin, R. In Vivo Approaches to Understand Arrhythmogenic Cardiomyopathy: Perspectives on Animal Models. Preprints2024, 2024061854. https://doi.org/10.20944/preprints202406.1854.v1
APA Style
Risato, G., Brañas Casas, R., Cason, M., Bueno Marinas, M., Pinci, S., De Gaspari, M., Visentin, S., Rizzo, S., Thiene, G., Basso, C., Pilichou, K., Tiso, N., & Celeghin, R. (2024). In Vivo Approaches to Understand Arrhythmogenic Cardiomyopathy: Perspectives on Animal Models. Preprints. https://doi.org/10.20944/preprints202406.1854.v1
Chicago/Turabian Style
Risato, G., Natascia Tiso and Rudy Celeghin. 2024 "In Vivo Approaches to Understand Arrhythmogenic Cardiomyopathy: Perspectives on Animal Models" Preprints. https://doi.org/10.20944/preprints202406.1854.v1
Abstract
Arrhythmogenic cardiomyopathy (AC) is a hereditary cardiac disorder characterized by the gradual replacement of cardiomyocytes with fibrous and adipose tissue, leading to ventricular wall thinning, chamber dilation, arrhythmias, and sudden cardiac death. Despite advances in treatment, disease management remains challenging. Animal models, particularly mice and zebrafish, have become invaluable tools for understanding AC's pathophysiology and testing potential therapies. Mice models, although useful for scientific research, cannot fully replicate the complexity of the human AC. However, they have provided valuable insights into gene involvement, signalling pathways, and disease progression. Zebrafish offer a promising alternative to mammalian models, despite the phylogenetic distance, due to their economic and genetic advantages. By combining animal models with in vitro studies, researchers can comprehensively understand AC, paving the way for more effective treatments and interventions for patients and improving their quality of life and prognosis.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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