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Volume 25
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Review

Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm

by
Yutang Wang
1,*,
Indu S. Panicker
1,
Jack Anesi
1,
Owen Sargisson
1,
Benjamin Atchison
1 and
Andreas J. R. Habenicht
2
1
Discipline of Life Science, Institute of Innovation, Science and Sustainability, Federation University Australia, Ballarat, VIC 3353, Australia
2
Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität München (LMU), 80336 Munich, Germany
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2024, 25(2), 901; https://doi.org/10.3390/ijms25020901
Submission received: 18 December 2023 / Revised: 3 January 2024 / Accepted: 9 January 2024 / Published: 11 January 2024
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)
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Abstract

Thoracic aortic aneurysm (TAA) has a prevalence of 0.16–0.34% and an incidence of 7.6 per 100,000 person-years, accounting for 1–2% of all deaths in Western countries. Currently, no effective pharmacological therapies have been identified to slow TAA development and prevent TAA rupture. Large TAAs are treated with open surgical repair and less invasive thoracic endovascular aortic repair, both of which have high perioperative mortality risk. Therefore, there is an urgent medical need to identify the cellular and molecular mechanisms underlying TAA development and rupture to develop new therapies. In this review, we summarize animal TAA models including recent developments in porcine and zebrafish models: porcine models can assess new therapeutic devices or intervention strategies in a large mammal and zebrafish models can employ large-scale small-molecule suppressor screening in microwells. The second part of the review covers current views of TAA pathogenesis, derived from recent studies using these animal models, with a focus on the roles of the transforming growth factor-beta (TGFβ) pathway and the vascular smooth muscle cell (VSMC)-elastin-contractile unit. The last part discusses TAA treatment options as they emerge from recent preclinical studies.
Keywords: Marfan syndrome; β-aminopropionitrile; calcium chloride; elastase; angiotensin II Marfan syndrome; β-aminopropionitrile; calcium chloride; elastase; angiotensin II

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MDPI and ACS Style

Wang, Y.; Panicker, I.S.; Anesi, J.; Sargisson, O.; Atchison, B.; Habenicht, A.J.R. Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm. Int. J. Mol. Sci. 2024, 25, 901. https://doi.org/10.3390/ijms25020901

AMA Style

Wang Y, Panicker IS, Anesi J, Sargisson O, Atchison B, Habenicht AJR. Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm. International Journal of Molecular Sciences. 2024; 25(2):901. https://doi.org/10.3390/ijms25020901

Chicago/Turabian Style

Wang, Yutang, Indu S. Panicker, Jack Anesi, Owen Sargisson, Benjamin Atchison, and Andreas J. R. Habenicht. 2024. "Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm" International Journal of Molecular Sciences 25, no. 2: 901. https://doi.org/10.3390/ijms25020901

APA Style

Wang, Y., Panicker, I. S., Anesi, J., Sargisson, O., Atchison, B., & Habenicht, A. J. R. (2024). Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm. International Journal of Molecular Sciences, 25(2), 901. https://doi.org/10.3390/ijms25020901

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