Abstract
Atherosclerosis (AS), as a chronic inflammatory disorder of the cardiovascular system, is one of the leading causes of ischemic heart disease, stroke and peripheral vascular disease. There is growing evidence on the role of innate and adaptive immunity in the pathogenesis of atherosclerosis. Interleukin-18 is one of the novel proinflammatory cytokines involved in atherogenesis, atherosclerotic plaque instability and plaque rupture. In this review, we overview the findings of preclinical and clinical studies about the role and mechanism of action of IL-18 in the pathogenesis of AS, which could offer novel prognostic and therapeutic approaches.
Highlights
Atherosclerosis (AS) is a chronic inflammatory disease resulting from a complex interaction of multiple biological pathways leading to the formation and progression of lipid-laden plaques in the wall of the arteries
These results demonstrate that IL-18 is as a proatherogenic cytokine which promotes the progression of IFN-γ secreting T helper 1 (Th1) cells [49]
This study demonstrates that IL-18R and Na-Cl co-transporter (NCC) in combination contribute to the atherogenesis and colocalize in vascular SMCs (VSMCs), endothelial cells (EC) and macrophages
Summary
Atherosclerosis (AS) is a chronic inflammatory disease resulting from a complex interaction of multiple biological pathways leading to the formation and progression of lipid-laden plaques in the wall of the arteries. It has been reported that IL-18−/−×apoE−/− mice have significantly reduced AS, local IFN-γ signaling and plaque rapture despite elevated serum cholesterol and triglyceride levels These results demonstrate that IL-18 is as a proatherogenic cytokine which promotes the progression of IFN-γ secreting Th1 cells [49]. OxLDL which acts by binding several scavenger receptors such as lectin-like oxLDL receptor-1 (LOX-1) is a type II membrane protein which participates in ligand binding [81, 82] These non-traditional receptors are mainly expressed on ECs, macrophages, monocytes, platelets, cardiomyocytes and VSMCs. LOX-1 is generally undetectable in physiological states, but it is over-expressed when exposed to different proinflammatory redox-sensitive transduction and proatherogenic stimulants and can be activated in vascular endothelial dysfunction [83-85].
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