Abstract
As a chronic inflammatory disease, atherosclerosis is a leading cause of morbidity and mortality in most countries. Inflammation is responsible for plaque instability and the subsequent onset of acute coronary syndrome (ACS), which is one of the leading causes of hospitalization. Therefore, exploring the potential mechanism underlying ACS is of considerable concern, and searching for alternative therapeutic targets is very urgent. Interleukin-37 (IL-37) inhibits the production of proinflammatory chemokines and cytokines and acts as a natural inhibitor of innate and adaptive immunity. Interestingly, our previous study with murine models showed that IL-37 alleviated cardiac remodeling and myocardial ischemia/reperfusion injury. Of note, our clinical study revealed that IL-37 is elevated and plays a beneficial role in patients with ACS. Moreover, dendritic cells (DCs) orchestrate both immunity and tolerance, and tolerogenic DCs (tDCs) are characterized by more secretion of immunosuppressive cytokines. As expected, IL-37-treated DCs are tolerogenic. Hence, we speculate that IL-37- or IL-37-treated DCs is a novel therapeutic possibility for ACS, and the precise mechanism of IL-37 requires further study.
Highlights
Atherosclerosis is a chronic inflammatory disease and the basis of acute coronary syndrome (ACS), including acute myocardial infarction and unstable angina [1]
Inflammatory reactions are triggered by the discharge of intracellular substances from necrotic myocardium after myocardial infarction (MI), followed by activation of nuclear factor- (NF-) κB, which is an essential transcription factor that controls the expression of inflammatory genes, such as chemokines and cytokines
We demonstrated that the inflammatory reactions inhibited by IL-37 were independent of the infarct size after MI by ruling out the influence of the secondary immune response due to the smaller infarct size [42]
Summary
Atherosclerosis is a chronic inflammatory disease and the basis of acute coronary syndrome (ACS), including acute myocardial infarction and unstable angina [1]. ACS is a result of coronary plaque erosion or rupture, where inflammation plays a central role [1,2,3]. Several clinical experiments have demonstrated that high-sensitivity Creactive protein (hs-CRP) is a biomarker of inflammation and atheromatous plaque vulnerability [5,6,7]. A previous publication showed that a poor clinical outcome after myocardial infarction (MI) can be predicted by increased serum CRP concentration [8]. We showed that hs-CRP levels were significantly higher in patients with ACS [9].
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