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NLRP3 炎性小体在动脉粥样硬化、冠心病和急性心肌梗死中的免疫调节作用。

Immunomodulation of the NLRP3 Inflammasome in Atherosclerosis, Coronary Artery Disease, and Acute Myocardial Infarction.

机构信息

Department of Cardiology, University Medical Center Utrecht, Heidelberglaan 100, 3508, GA, Utrecht, The Netherlands.

Department of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands.

出版信息

J Cardiovasc Transl Res. 2021 Feb;14(1):23-34. doi: 10.1007/s12265-020-10049-w. Epub 2020 Jul 9.

DOI:10.1007/s12265-020-10049-w
PMID:32648087
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7892681/
Abstract

Cardiovascular disease (CVD) remains the leading cause of mortality and morbidity worldwide. Atherosclerosis is responsible for the majority of cardiovascular disorders with inflammation as one of its driving processes. The nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, responsible for the release of the pro-inflammatory cytokines, interleukin-1β (IL-1β), and interleukin-18 (IL-18), has been studied extensively and showed to play a pivotal role in the progression of atherosclerosis, coronary artery disease (CAD), and myocardial ischemia reperfusion (I/R) injury. Both the NLRP3 inflammasome and its downstream cytokines, IL-1ß and IL-18, could therefore be promising targets in cardiovascular disease. This review summarizes the role of the NLRP3 inflammasome in atherosclerosis, CAD, and myocardial I/R injury. Furthermore, the current therapeutic approaches targeting the NLRP3 inflammasome and its downstream signaling cascade in atherosclerosis, CAD, and myocardial I/R injury are discussed.

摘要

心血管疾病 (CVD) 仍然是全球死亡和发病的主要原因。动脉粥样硬化是大多数心血管疾病的原因，炎症是其驱动过程之一。核苷酸结合寡聚化结构域样受体家族含pyrin 结构域蛋白 3 (NLRP3) 炎性小体负责释放促炎细胞因子白细胞介素-1β (IL-1β) 和白细胞介素-18 (IL-18)，已经得到了广泛的研究，并显示在动脉粥样硬化、冠心病 (CAD) 和心肌缺血再灌注 (I/R) 损伤的进展中发挥关键作用。NLRP3 炎性小体及其下游细胞因子 IL-1β 和 IL-18 因此可能是心血管疾病的有前途的靶点。本文综述了 NLRP3 炎性小体在动脉粥样硬化、CAD 和心肌 I/R 损伤中的作用。此外，还讨论了针对 NLRP3 炎性小体及其下游信号级联在动脉粥样硬化、CAD 和心肌 I/R 损伤中的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d6a/7892681/2d6b3b46c037/12265_2020_10049_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d6a/7892681/30601e2773c4/12265_2020_10049_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d6a/7892681/93865fc97037/12265_2020_10049_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d6a/7892681/2d6b3b46c037/12265_2020_10049_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d6a/7892681/30601e2773c4/12265_2020_10049_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d6a/7892681/93865fc97037/12265_2020_10049_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d6a/7892681/2d6b3b46c037/12265_2020_10049_Fig3_HTML.jpg

相似文献

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[3]
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[8]
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[2]
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J Med Biochem. 2025-6-13

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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction.

N Engl J Med. 2019-11-16

[2]
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Eur Heart J. 2020-1-14

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Residual inflammatory risk associated with interleukin-18 and interleukin-6 after successful interleukin-1β inhibition with canakinumab: further rationale for the development of targeted anti-cytokine therapies for the treatment of atherothrombosis.

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J Cardiovasc Pharmacol. 2019-9

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J Cardiovasc Pharmacol. 2019-10

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Int J Mol Sci. 2019-7-6

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Cardiovasc Res. 2019-7-1

[9]
The NLRP3 inflammasome: molecular activation and regulation to therapeutics.

Nat Rev Immunol. 2019-8

[10]
The NLRP3 Inflammasome Inhibitor, OLT1177 (Dapansutrile), Reduces Infarct Size and Preserves Contractile Function After Ischemia Reperfusion Injury in the Mouse.

J Cardiovasc Pharmacol. 2019-4

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