详细信息
Clinical Implications of IL-32, IL-34 and IL-37 in Atherosclerosis: Speculative Role in Cardiovascular Manifestations of COVID-19 ( SCI-EXPANDED收录) 被引量:18
文献类型:期刊文献
英文题名:Clinical Implications of IL-32, IL-34 and IL-37 in Atherosclerosis: Speculative Role in Cardiovascular Manifestations of COVID-19
作者:Law, Ching Chee[1];Puranik, Rajesh[2];Fan, Jingchun[3];Fei, Jian[4];Hambly, Brett D.[1];Bao, Shisan[1]
第一作者:Law, Ching Chee
通信作者:Bao, SS[1];Fei, J[2]
机构:[1]Univ Sydney, Sch Biomed Engn, Sydney, NSW, Australia;[2]Royal Prince Alfred Hosp, Dept Cardiol, Sydney, NSW, Australia;[3]Gansu Univ Chinese Med, Sch Publ Hlth, Lanzhou, Peoples R China;[4]SMOC, Shanghai Engn Res Ctr Model Organisms, Shanghai, Peoples R China
第一机构:Univ Sydney, Sch Biomed Engn, Sydney, NSW, Australia
通信机构:[1]corresponding author), Univ Sydney, Sch Biomed Engn, Sydney, NSW, Australia;[2]corresponding author), SMOC, Shanghai Engn Res Ctr Model Organisms, Shanghai, Peoples R China.
年份:2021
卷号:8
外文期刊名:FRONTIERS IN CARDIOVASCULAR MEDICINE
收录:;Scopus(收录号:2-s2.0-85172295053);WOS:【SCI-EXPANDED(收录号:WOS:000684737200002)】;
基金:We acknowledge the supporters from SJTU research grant 2019 at the University of Sydney and Science and Technology Commission of Shanghai Municipality (19DZ2280500).
语种:英文
外文关键词:IL-32; IL-34; IL-37; implication; COVID-19
摘要:Atherosclerosis, which is a primary cause of cardiovascular disease (CVD) deaths around the world, is a chronic inflammatory disease that is characterised by the accumulation of lipid plaques in the arterial wall, triggering inflammation that is regulated by cytokines/chemokines that mediate innate and adaptive immunity. This review focuses on IL-32, -34 and -37 in the stable vs. unstable plaques from atherosclerotic patients. Dysregulation of the novel cytokines IL-32, -34 and -37 has been discovered in atherosclerotic plaques. IL-32 and -34 are pro-atherogenic and associated with an unstable plaque phenotype; whereas IL-37 is anti-atherogenic and maintains plaque stability. It is speculated that these cytokines may contribute to the explanation for the increased occurrence of atherosclerotic plaque rupture seen in patients with COVID-19 infection. Understanding the roles of these cytokines in atherogenesis may provide future therapeutic perspectives, both in the management of unstable plaque and acute coronary syndrome, and may contribute to our understanding of the COVID-19 cytokine storm.
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