title: Mouse models of atherosclerosis: a historical perspective and recent advances.
abstract: 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.
authors.affiliation: School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, SAR, People's Republic of China.
authors.forename: Yee Ting
authors.initials: YT
authors.lastname: Lee
authors.affiliation: School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, SAR, People's Republic of China.
authors.forename: Hiu Yu
authors.initials: HY
authors.lastname: Lin
authors.affiliation: School of Biological Sciences, University of Cambridge, Cambridge, UK.
authors.forename: Yin Wah Fiona
authors.initials: YW
authors.lastname: Chan
authors.affiliation: Faculty of Medicine, Newcastle University, Newcastle, UK.
authors.forename: Ka Hou Christien
authors.initials: KH
authors.lastname: Li
authors.affiliation: Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong, SAR, People's Republic of China.
authors.forename: Olivia Tsz Ling
authors.initials: OT
authors.lastname: To
authors.affiliation: Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong, SAR, People's Republic of China.|Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia.
authors.forename: Bryan P
authors.initials: BP
authors.lastname: Yan
authors.affiliation: Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China.
authors.forename: Tong
authors.initials: T
authors.lastname: Liu
authors.affiliation: Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China.
authors.forename: Guangping
authors.initials: G
authors.lastname: Li
authors.affiliation: School of Life Sciences, Chinese University of Hong Kong, Hong Kong, SAR, People's Republic of China.
authors.forename: Wing Tak
authors.initials: WT
authors.lastname: Wong
authors.affiliation: Stem Cell & Regenerative Medicine Consortium, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, SAR, People's Republic of China.
authors.forename: Wendy
authors.initials: W
authors.lastname: Keung
authors.affiliation: Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong, SAR, People's Republic of China. tseg@cuhk.edu.hk.|Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong, SAR, People's Republic of China. tseg@cuhk.edu.hk.
authors.forename: Gary
authors.identifier: http://orcid.org/0000-0001-5510-1253
authors.initials: G
authors.lastname: Tse
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D004249:DNA Damage; D004272:DNA, Mitochondrial; D004195:Disease Models, Animal; D059865:Endoplasmic Reticulum Stress; D007249:Inflammation / Q000188:drug therapy; D051379:Mice; D018384:Oxidative Stress
chemical_list: D004272:DNA, Mitochondrial
keywords: ApoE; Atherosclerosis; ER stress; LDL receptor; Mitochondrial dysfunction; Mouse models; Reactive oxygen species