Cerebrovascular disease and coronary artery disease (CAD) are the most prevalent subtypes of cardiovascular disease that result in a high morbidity as well as large economic burden in developing countries ( 1). 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.Ĭardiovascular disease (CVD) is the leading cause of death in the world ( 1). 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. IL-32 and -34 are pro-atherogenic and associated with an unstable plaque phenotype whereas IL-37 is anti-atherogenic and maintains plaque stability. Dysregulation of the novel cytokines IL-32, -34 and -37 has been discovered in atherosclerotic plaques. unstable plaques from atherosclerotic patients. This review focuses on IL-32, -34 and -37 in the stable vs.

4Shanghai Engineering Research Centre for Model Organisms, SMOC, Shanghai, ChinaĪtherosclerosis, 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.3School of Public Health, Gansu University of Chinese Medicine, Lanzhou, China.2Department of Cardiology, Royal Prince Alfred Hospital, Sydney, NSW, Australia.1School of Biomedical Engineering, The University of Sydney, Sydney, NSW, Australia.Ching Chee Law 1, Rajesh Puranik 2, Jingchun Fan 3, Jian Fei 4 *, Brett D.

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