Chronic inflammation caused by immune cells and their mediators is a characteristic of atherosclerosis. Interleukin-38 (IL-38), a member of the IL-1 family, exerts multiple anti-inflammatory effects via specific ligand-receptor interactions. Upon recognizing a specific receptor, IL-38 restrains mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NK-κB), or other inflammation-related signaling pathways in inflammatory disease. Further research has shown that IL-38 also displays anti-atherosclerotic effects and reduces the occurrence and risk of cardiovascular events. On the one hand, IL-38 can regulate innate and adaptive immunity to inhibit inflammation, reduce pathological neovascularization, and inhibit apoptosis. On the other hand, it can curb obesity, reduce hyperlipidemia, and restrain insulin resistance to reduce cardiovascular disease risk. Therefore, this article expounds on the vital function of IL-38 in the development of atherosclerosis to provide a theoretical basis for further in-depth studies of IL-38 and insights on the prophylaxis and treatment of atherosclerosis.
Keywords: Atherosclerosis; Hyperlipidemia; Inflammation; Macrophages; Th17 cells; Tregs; interleukin-38.
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