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Mouse models of atherosclerosis: a historical perspective and recent advances

Atherosclerosis represents a significant cause of morbidity and mortality in both the developed and developing countries. Animal models of atherosclerosis have served as valuable tools for providing insights on its aetiology, pathophysiology and complications. They can be used for invasive interroga...

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Autores principales: Lee, Yee Ting, Lin, Hiu Yu, Chan, Yin Wah Fiona, Li, Ka Hou Christien, To, Olivia Tsz Ling, Yan, Bryan P, Liu, Tong, Li, Guangping, Wong, Wing Tak, Keung, Wendy, Tse, Gary
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5240327/
https://www.ncbi.nlm.nih.gov/pubmed/28095860
http://dx.doi.org/10.1186/s12944-016-0402-5
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author Lee, Yee Ting
Lin, Hiu Yu
Chan, Yin Wah Fiona
Li, Ka Hou Christien
To, Olivia Tsz Ling
Yan, Bryan P
Liu, Tong
Li, Guangping
Wong, Wing Tak
Keung, Wendy
Tse, Gary
author_facet Lee, Yee Ting
Lin, Hiu Yu
Chan, Yin Wah Fiona
Li, Ka Hou Christien
To, Olivia Tsz Ling
Yan, Bryan P
Liu, Tong
Li, Guangping
Wong, Wing Tak
Keung, Wendy
Tse, Gary
author_sort Lee, Yee Ting
collection PubMed
description Atherosclerosis represents a significant cause of morbidity and mortality in both the developed and developing countries. Animal models of atherosclerosis have served as valuable tools for providing insights on its aetiology, pathophysiology and complications. They can be used for invasive interrogation of physiological function and provide a platform for testing the efficacy and safety of different pharmacological therapies. Compared to studies using human subjects, animal models have the advantages of being easier to manage, with controllable diet and environmental risk factors. Moreover, pathophysiological changes can be induced either genetically or pharmacologically to study the harmful effects of these interventions. There is no single ideal animal model, as different systems are suitable for different research objectives. A good understanding of the similarities and differences to humans enables effective extrapolation of data for translational application. In this article, we will examine the different mouse models for the study and elucidation of the pathophysiological mechanisms underlying atherosclerosis. We also review recent advances in the field, such as the role of oxidative stress in promoting endoplasmic reticulum stress, mitochondrial dysfunction and mitochondrial DNA damage, which can result in vascular inflammation and atherosclerosis. Finally, novel therapeutic approaches to reduce vascular damage caused by chronic inflammation using microRNA and nano-medicine technology, are discussed.
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spelling pubmed-52403272017-01-23 Mouse models of atherosclerosis: a historical perspective and recent advances Lee, Yee Ting Lin, Hiu Yu Chan, Yin Wah Fiona Li, Ka Hou Christien To, Olivia Tsz Ling Yan, Bryan P Liu, Tong Li, Guangping Wong, Wing Tak Keung, Wendy Tse, Gary Lipids Health Dis Review Atherosclerosis represents a significant cause of morbidity and mortality in both the developed and developing countries. Animal models of atherosclerosis have served as valuable tools for providing insights on its aetiology, pathophysiology and complications. They can be used for invasive interrogation of physiological function and provide a platform for testing the efficacy and safety of different pharmacological therapies. Compared to studies using human subjects, animal models have the advantages of being easier to manage, with controllable diet and environmental risk factors. Moreover, pathophysiological changes can be induced either genetically or pharmacologically to study the harmful effects of these interventions. There is no single ideal animal model, as different systems are suitable for different research objectives. A good understanding of the similarities and differences to humans enables effective extrapolation of data for translational application. In this article, we will examine the different mouse models for the study and elucidation of the pathophysiological mechanisms underlying atherosclerosis. We also review recent advances in the field, such as the role of oxidative stress in promoting endoplasmic reticulum stress, mitochondrial dysfunction and mitochondrial DNA damage, which can result in vascular inflammation and atherosclerosis. Finally, novel therapeutic approaches to reduce vascular damage caused by chronic inflammation using microRNA and nano-medicine technology, are discussed. BioMed Central 2017-01-17 /pmc/articles/PMC5240327/ /pubmed/28095860 http://dx.doi.org/10.1186/s12944-016-0402-5 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Lee, Yee Ting
Lin, Hiu Yu
Chan, Yin Wah Fiona
Li, Ka Hou Christien
To, Olivia Tsz Ling
Yan, Bryan P
Liu, Tong
Li, Guangping
Wong, Wing Tak
Keung, Wendy
Tse, Gary
Mouse models of atherosclerosis: a historical perspective and recent advances
title Mouse models of atherosclerosis: a historical perspective and recent advances
title_full Mouse models of atherosclerosis: a historical perspective and recent advances
title_fullStr Mouse models of atherosclerosis: a historical perspective and recent advances
title_full_unstemmed Mouse models of atherosclerosis: a historical perspective and recent advances
title_short Mouse models of atherosclerosis: a historical perspective and recent advances
title_sort mouse models of atherosclerosis: a historical perspective and recent advances
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5240327/
https://www.ncbi.nlm.nih.gov/pubmed/28095860
http://dx.doi.org/10.1186/s12944-016-0402-5
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