Abstract
AbstractAtherosclerosis is characterized by the development of intimal plaque, thrombosis, and stenosis of the vessel lumen causing decreased blood flow and hypoxia precipitating angina. Chronic inflammation in the stable plaque renders it unstable and rupture of unstable plaques results in the formation of emboli leading to hypoxia/ischemia to the organs by occluding the terminal branches and precipitate myocardial infarction and stroke. Such delibitating events could be controlled by the strategies that prevent plaque development or plaque stabilization. Despite the use of statins to stabilize plaques, there is a need for novel targets due to continuously increasing cases of cardiovascular events. Sirtuins (SIRTs), a family of signaling proteins, are involved in sustaining genome integrity, DNA damage response and repair, modulating oxidative stress, aging, inflammation, and energy metabolism. SIRTs play a critical role in modulating inflammation and involves in the development and progression of atherosclerosis. The role of SIRTs in relation to atherosclerosis and plaque vulnerability is scarcely discussed in the literature. Since SIRTs regulate oxidative stress, inflammation, and aging, they may also regulate plaque progression and vulnerability as these molecular mechanisms underlie the pathogenesis of plaque development, progression, and vulnerability. This review critically discusses the role of SIRTs in plaque progression and vulnerability and the possibility of targeting SIRTs to attenuate plaque rupture, focusing on the highlights in genomics, molecular pathways, and cell types involved in the underlying pathophysiology.
Funder
National Institutes of Health
Western University of Health Sciences
Publisher
Springer Science and Business Media LLC
Subject
Cell Biology,Clinical Biochemistry,Molecular Biology,General Medicine
Reference103 articles.
1. Murray CJL, Phil D, Lopez AD (2013) Measuring the global burden of disease. New Engl J Med 369(5):448–457
2. Organization WH. Cardiovascular diseases (CVDs). Fact sheet. Reviewed June 2016. cited 2016-08-26. http://www.who.int/mediacentre/factsheets/fs317/en
3. Herrington W, Lacey B, Sherilkar P, Armitage J, Lewington S (2016) Epidemiology of atherosclerosis and the potential to reduce the global burden of atherothrombotic disease. Circ Res AHA J 118(4):535–546
4. Bentzon JF, Otsuka F, Virmani R, Falk E (2014) Mechanisms of plaque formation and rupture. Circ Res AHA J 114(12):1852–1866
5. Hafiane A (2019) Vulnerable plaque, characteristics, detection, and potential therapies. J Cardiovasc Dev Dis 6(3)
Cited by
1 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献