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动脉粥样硬化中的NLRP3炎性小体：机制与靶向治疗

NLRP3 inflammasome in atherosclerosis: Mechanisms and targeted therapies.

作者信息

Chen Pengfei, Li Xia

机构信息

Marine College, Shandong University, Weihai, China.

Shandong Kelun Pharmaceutical Co, Ltd., Binzhou, China.

出版信息

Front Pharmacol. 2024 Jul 31;15:1430236. doi: 10.3389/fphar.2024.1430236. eCollection 2024.

DOI:10.3389/fphar.2024.1430236
PMID:39144618
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11322363/
Abstract

Atherosclerosis (AS) is the primary pathology behind various cardiovascular diseases and the leading cause of death and disability globally. Recent evidence suggests that AS is a chronic vascular inflammatory disease caused by multiple factors. In this context, the NLRP3 inflammasome, acting as a signal transducer of the immune system, plays a critical role in the onset and progression of AS. The NLRP3 inflammasome is involved in endothelial injury, foam cell formation, and pyroptosis in AS. Therefore, targeting the NLRP3 inflammasome offers a new treatment strategy for AS. This review highlights the latest insights into AS pathogenesis and the pharmacological therapies targeting the NLRP3 inflammasome, focusing on optimal targets for small molecule inhibitors. These insights are valuable for rational drug design and the pharmacological assessment of new targeted NLRP3 inflammasome inhibitors in treating AS.

摘要

动脉粥样硬化（AS）是各种心血管疾病背后的主要病理机制，也是全球死亡和残疾的主要原因。最近的证据表明，AS是一种由多种因素引起的慢性血管炎症性疾病。在这种情况下，作为免疫系统信号转导器的NLRP3炎性小体在AS的发生和发展中起关键作用。NLRP3炎性小体参与AS中的内皮损伤、泡沫细胞形成和细胞焦亡。因此，靶向NLRP3炎性小体为AS提供了一种新的治疗策略。本综述重点介绍了AS发病机制的最新见解以及针对NLRP3炎性小体的药物治疗，重点关注小分子抑制剂的最佳靶点。这些见解对于合理的药物设计以及新型靶向NLRP3炎性小体抑制剂治疗AS的药理学评估具有重要价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/e641cda77b90/fphar-15-1430236-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/eb9411b0461e/fphar-15-1430236-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/2e9494a90b63/fphar-15-1430236-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/0470fa9888e6/fphar-15-1430236-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/f25856e1c8ea/fphar-15-1430236-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/b08effab2c8b/fphar-15-1430236-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/87988f1bc401/fphar-15-1430236-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/e641cda77b90/fphar-15-1430236-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/eb9411b0461e/fphar-15-1430236-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/2e9494a90b63/fphar-15-1430236-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/0470fa9888e6/fphar-15-1430236-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/f25856e1c8ea/fphar-15-1430236-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/b08effab2c8b/fphar-15-1430236-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/87988f1bc401/fphar-15-1430236-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ceb/11322363/e641cda77b90/fphar-15-1430236-g007.jpg

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NLRP3 inflammasome in atherosclerosis: Mechanisms and targeted therapies.

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引用本文的文献

[1]
NLRP3-Mediated PANoptosis and Associated Interventions in Endothelial Injury.

Cardiovasc Toxicol. 2025-6-18

[2]
The Anti-Inflammatory Potential of Tricyclic Antidepressants (TCAs): A Novel Therapeutic Approach to Atherosclerosis Pathophysiology.

Pharmaceuticals (Basel). 2025-1-31

[3]
Global Research Trends and Focus on the Link Between Heart Failure and NLRP3 Inflammasome: A Bibliometric Analysis From 2010 to 2024.

J Multidiscip Healthc. 2025-2-8

[4]
"Anti-inflammatory Therapies in Atherosclerosis - Where are we going?".

Curr Atheroscler Rep. 2024-12-19

本文引用的文献

[1]
Discovery of novel biphenyl-sulfonamide analogues as NLRP3 inflammasome inhibitors.

Bioorg Chem. 2024-5

[2]
Brazilin is a natural product inhibitor of the NLRP3 inflammasome.

iScience. 2024-1-19

[3]
Global Burden of Cardiovascular Diseases and Risks, 1990-2022.

J Am Coll Cardiol. 2023-12-19

[4]
Drugging the NLRP3 inflammasome: from signalling mechanisms to therapeutic targets.

Nat Rev Drug Discov. 2024-1

[5]
Multiple TLRs elicit alternative NLRP3 inflammasome activation in primary human monocytes independent of RIPK1 kinase activity.

Front Immunol. 2023

[6]
Novel Sulfonylurea-Based NLRP3 Inflammasome Inhibitor for Efficient Treatment of Nonalcoholic Steatohepatitis, Endotoxic Shock, and Colitis.

J Med Chem. 2023-9-28

[7]
Mechanisms of fibrous cap formation in atherosclerosis.

Front Cardiovasc Med. 2023-8-21

[8]
Smooth muscle liver kinase B1 inhibits foam cell formation and atherosclerosis via direct phosphorylation and activation of SIRT6.

Cell Death Dis. 2023-8-22

[9]
JT002, a small molecule inhibitor of the NLRP3 inflammasome for the treatment of autoinflammatory disorders.

Sci Rep. 2023-8-19

[10]
Regulation of toll-like receptor (TLR) signaling pathways in atherosclerosis: from mechanisms to targeted therapeutics.

Acta Pharmacol Sin. 2023-12

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