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NLRP3 inflammasome in cardiovascular diseases: an update.

作者信息

Mo Binhai, Ding Yudi, Ji Qingwei

机构信息

People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.

First People's Hospital of Nanning, Nanning, Guangxi, China.

出版信息

Front Immunol. 2025 Feb 26;16:1550226. doi: 10.3389/fimmu.2025.1550226. eCollection 2025.


DOI:10.3389/fimmu.2025.1550226
PMID:40079000
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11896874/
Abstract

Cardiovascular disease (CVD) continues to be the leading cause of mortality worldwide. The nucleotide oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3 (NLRP3) inflammasome is involved in numerous types of CVD. As part of innate immunity, the NLRP3 inflammasome plays a vital role, requiring priming and activation signals to trigger inflammation. The NLRP3 inflammasome leads both to the release of IL-1 family cytokines and to a distinct form of programmed cell death called pyroptosis. Inflammation related to CVD has been extensively investigated in relation to the NLRP3 inflammasome. In this review, we describe the pathways triggering NLRP3 priming and activation and discuss its pathogenic effects on CVD. This study also provides an overview of potential therapeutic approaches targeting the NLRP3 inflammasome.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a67e/11896874/2b9b31a88581/fimmu-16-1550226-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a67e/11896874/728eb9566bfb/fimmu-16-1550226-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a67e/11896874/2b9b31a88581/fimmu-16-1550226-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a67e/11896874/728eb9566bfb/fimmu-16-1550226-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a67e/11896874/2b9b31a88581/fimmu-16-1550226-g002.jpg

相似文献

[1]
NLRP3 inflammasome in cardiovascular diseases: an update.

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[2]
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[3]
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[4]
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Am J Respir Cell Mol Biol. 2016-2

[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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引用本文的文献

[1]
The gut-heart axis: a correlation between Paneth cells' dysfunction, microbiome dysbiosis, and cardiovascular diseases.

Cell Commun Signal. 2025-7-18

[2]
Inflammasome Signaling in Cardiac Arrhythmias: Linking Inflammation, Fibrosis, and Electrical Remodeling.

Int J Mol Sci. 2025-6-20

本文引用的文献

[1]
Time-of-day control of mitochondria regulates NLRP3 inflammasome activation in macrophages.

FASEB J. 2024-12-13

[2]
Targeting the smooth muscle cell Keap1-Nrf2-GSDMD-pyroptosis axis by cryptotanshinone prevents abdominal aortic aneurysm formation.

Theranostics. 2024

[3]
Effects of Catheter-Based Renal Denervation in Hypertension: A Systematic Review and Meta-Analysis.

Circulation. 2024-11-12

[4]
Urinary Metal Levels and Coronary Artery Calcification: Longitudinal Evidence in the Multi-Ethnic Study of Atherosclerosis.

J Am Coll Cardiol. 2024-10-15

[5]
Inhibitors of NLRP3 Inflammasome Formation: A Cardioprotective Role for the Gasotransmitters Carbon Monoxide, Nitric Oxide, and Hydrogen Sulphide in Acute Myocardial Infarction.

Int J Mol Sci. 2024-8-26

[6]
Glyburide use is associated with a greater likelihood of mortality or rehospitalization after acute coronary syndrome compared to gliclazide use in adults with type 2 diabetes: A cohort study.

Diabetes Obes Metab. 2024-11

[7]
Prediction of Cumulative Exposure to Atherogenic Lipids During Early Adulthood.

J Am Coll Cardiol. 2024-9-10

[8]
Demonstration of the Protective Effect of Vinpocetine in Diabetic Cardiomyopathy.

J Clin Med. 2024-8-8

[9]
APOE-NOTCH axis governs elastogenesis during human cardiac valve remodeling.

Nat Cardiovasc Res. 2024-8

[10]
Th1 cells reduce the osteoblast-like phenotype in valvular interstitial cells by inhibiting NLRP3 inflammasome activation in macrophages.

Mol Med. 2024-7-30

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