Role of IL‐37‐ and IL‐37‐Treated Dendritic Cells in Acute Coronary Syndrome

Zhu, Ruirui; Zhang, Fangyuan; Pan, Chengliang; Yu, Kunwu; Zhong, Yucheng; Zeng, Qiutang

doi:10.1155/2021/6454177

Cited by 8 publications

(12 citation statements)

References 101 publications

(151 reference statements)

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“… 62 , 63 IL-37 also mediated lipid metabolism via the IL-1R8/TLR4/NF-κB signaling pathway to reduce MI. 64 In conclusion, IL-37 influences CD4+ T cell typing, promotes macrophage transformation and regulates lipid metabolism during MI. The IL-37 amplification of Tregs is similar to the IL-33/ST2 signaling pathway and research is necessary to demonstrate whether these two cytokines engage in cross-talk.…”

Section: Regulation Of Interleukin-1 Family In Cardiovascular Diseasesmentioning

confidence: 94%

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Progress of Research into the Interleukin-1 Family in Cardiovascular Disease

Wu¹,

Luo²,

Zheng³

2022

JIR

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Inflammatory factors, such as the IL-1 family, are generally acknowledged to be involved in systemic diseases and IL-1α and IL-1β, in particular, have been linked to cardiovascular disease with IL-18, IL-33, IL-36, IL-37 and IL-38 yet to be explored. The current review aims to summarize mechanisms of IL-18, IL-33, IL-36, IL-37 and IL-38 in myocardial infarction, hypertension, arrhythmia, valvular disease and aneurysm and to explore the potential for cardiovascular disease treatment strategies and discuss future directions for prevention and treatment.

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Section: Regulation Of Interleukin-1 Family In Cardiovascular Diseasesmentioning

confidence: 94%

Section: Myocardial Infarctionmentioning

confidence: 94%

Progress of Research into the Interleukin-1 Family in Cardiovascular Disease

Wu¹,

Luo²,

Zheng³

2022

JIR

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“…Excessive effective T cells and insufficient recruitment of Treg cells can lead to malignant ventricular remodeling after MI (68). The ability of IL-37-induced DCs to activate naive T cells and induce Treg cells has been reported (69), whereas tolerant DCs induced by IL-38 and TnI show stronger tolerance (10). We found that IL-38 inhibited LPS-induced maturation of DCs, thus resulting in lower expression of cell surface molecules and inflammatory factors than that in LPS-induced DCs that were not treated with IL-38 (10).…”

Section: Interleukin-38 Ameliorates Malignant Ventricular Remodeling ...mentioning

confidence: 99%

Effects of IL-38 on Macrophages and Myocardial Ischemic Injury

Ding

Peng

et al. 2022

Front. Immunol.

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Macrophages play an important role in clearing necrotic myocardial tissues, myocardial ischemia–reperfusion injury, and ventricular remodeling after myocardial infarction. M1 macrophages not only participate in the inflammatory response in myocardial tissues after infarction, which causes heart damage, but also exert a protective effect on the heart during ischemia. In contrast, M2 macrophages exhibit anti-inflammatory and tissue repair properties by inducing the production of high levels of anti-inflammatory cytokines and fibro-progenitor cells. Interleukin (IL)-38, a new member of the IL-1 family, has been reported to modulate the IL-36 signaling pathway by playing a role similar to that of the IL-36 receptor antagonist, which also affects the production and secretion of macrophage-related inflammatory factors that play an anti-inflammatory role. IL-38 can relieve myocardial ischemia–reperfusion injury by promoting the differentiation of M1 macrophages into M2 macrophages, inhibit the activation of NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome, and increase the secretion of anti-inflammatory cytokines, such as IL-10 and transforming growth factor-β. The intact recombinant IL-38 can also bind to interleukin 1 receptor accessory protein-like 1 (IL-1RAPL1) to activate the c-jun N-terminal kinase/activator protein 1 (JNK/AP1) pathway and increase the production of IL-6. In addition, IL-38 regulates dendritic cell-induced cardiac regulatory T cells, thereby regulating macrophage polarization and improving ventricular remodeling after myocardial infarction. Accordingly, we speculated that IL-38 and macrophage regulation may be therapeutic targets for ameliorating myocardial ischemic injury and ventricular remodeling after myocardial infarction. However, the specific mechanism of the IL-38 action warrants further investigation.

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“…Furthermore, it was also reported that overexpression of IL-37 significantly increases plaque instability in ApoE -/- mice ( 14 ). Furthermore, in vitro experiments demonstrated that IL-37 attenuated atherosclerosis by suppressing T cell activation, inducing the response of regulatory T cells and inhibiting vascular calcification ( 11 , 15-17 ). However, to the best of our knowledge, the effect and underlying mechanism of IL-37 on diabetic atherosclerosis remains unclear.…”

Section: Introductionmentioning

confidence: 99%

IL‑37 suppresses macrophage ferroptosis to attenuate diabetic atherosclerosis via the NRF2 pathway

Xia

Zhao

et al. 2023

Exp Ther Med

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IL-37 is a newly discovered inflammatory factor. However, the protective effect and underlying mechanisms of IL-37 on atherosclerosis remain unclear. In the present study, IL-37 was used for intraperitoneal injection in diabetic ApoE -/- mice caused by streptozotocin. High glucose (HG)/ox-LDL was used to stimulate THP-1 original macrophage followed by IL-37 pretreatment in vitro . The atheromatous plaque area, oxidative stress and inflammation levels in ApoE -/- mice were evaluated, and the level of macrophage ferroptosis was detected in vivo and in vitro . It was identified that IL-37 treatment significantly decreased plaque area in diabetic ApoE -/- mice. IL-37 not only improved blood lipid levels in mice, but also reduced serum levels of inflammatory factors including IL-1β and IL-18. Furthermore, IL-37 increased GPX4 and nuclear factor erythroid 2-related factor 2 (NRF2) in the aorta of diabetic mice. In vitro experiment revealed that IL-37 inhibited HG/ox-LDL-induced ferroptosis in macrophages, as evidenced by improved cell membrane oxidation, reduced malondialdehyde production and increased GPX4 expression. Moreover, it was also found that IL-37 enhanced the nuclear translocation of NRF2 in macrophages, while ML385, a specific NRF2 inhibitor, significantly attenuated the protective effect of IL-37 on macrophage ferroptosis caused by HG/ox-LDL. In conclusion, IL-37 suppressed macrophage ferroptosis to attenuate atherosclerosis progression via activating the NRF2 pathway.

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Role of IL‐37‐ and IL‐37‐Treated Dendritic Cells in Acute Coronary Syndrome

Cited by 8 publications

References 101 publications

Progress of Research into the Interleukin-1 Family in Cardiovascular Disease

Progress of Research into the Interleukin-1 Family in Cardiovascular Disease

Effects of IL-38 on Macrophages and Myocardial Ischemic Injury

IL‑37 suppresses macrophage ferroptosis to attenuate diabetic atherosclerosis via the NRF2 pathway

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