NLRP3: A Novel Mediator in Cardiovascular Disease

Cardiovascular disease is a major cause of death worldwide. Inflammasome infiltration has been identified to play a central role in the pathological progression of certain cardiovascular diseases, such as vascular damage spanning atherosclerosis, aneurysm, or arteritis; ischemic heart disease; and o...

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Main Authors: Wenyi Zhou, Chunyuan Chen, Zhiheng Chen, Lin Liu, Jie Jiang, Zhixiang Wu, Mingyi Zhao, Yanfang Chen
Format: Article
Language:English
Published: Wiley 2018-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2018/5702103
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author Wenyi Zhou
Chunyuan Chen
Zhiheng Chen
Lin Liu
Jie Jiang
Zhixiang Wu
Mingyi Zhao
Yanfang Chen
author_facet Wenyi Zhou
Chunyuan Chen
Zhiheng Chen
Lin Liu
Jie Jiang
Zhixiang Wu
Mingyi Zhao
Yanfang Chen
author_sort Wenyi Zhou
collection DOAJ
description Cardiovascular disease is a major cause of death worldwide. Inflammasome infiltration has been identified to play a central role in the pathological progression of certain cardiovascular diseases, such as vascular damage spanning atherosclerosis, aneurysm, or arteritis; ischemic heart disease; and other nonischemic heart diseases including diabetic cardiomyopathy, chronic heart failure, and hypertension- or virus-induced cardiac dysfunction. The NLRP3 inflammasome, a key participant in the innate immune response, requires both priming and activation signals for the initiation of inflammation. Piling evidence has revealed that the NLRP3 inflammasome could exert an inflammatory effect by inducing the secretion of proinflammatory cytokines (i.e., IL-1β, IL-18) or could cause pyroptosis, a novel programmed cell death process, in a caspase-1-dependent manner. The importance of the NLRP3 inflammasome in cardiac disease has been broadly investigated. In this review, we present the current knowledge regarding the function of NLRP in vascular disease, ischemic heart disease, and nonischemic heart disease and discuss the potential therapeutic options targeting the NLRP3 inflammasome.
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language English
publishDate 2018-01-01
publisher Wiley
record_format Article
series Journal of Immunology Research
spelling doaj-art-3ac0ee80669f4acd8d5b19cc34d1a8512025-08-20T03:55:40ZengWileyJournal of Immunology Research2314-88612314-71562018-01-01201810.1155/2018/57021035702103NLRP3: A Novel Mediator in Cardiovascular DiseaseWenyi Zhou0Chunyuan Chen1Zhiheng Chen2Lin Liu3Jie Jiang4Zhixiang Wu5Mingyi Zhao6Yanfang Chen7Cardiovascular Department, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease, Guangzhou 510000, ChinaDepartment of Pediatrics, The Third Xiangya Hospital, Central South University, Changsha 410013, ChinaDepartment of Pediatrics, The Third Xiangya Hospital, Central South University, Changsha 410013, ChinaDepartment of Pediatrics, The Third Xiangya Hospital, Central South University, Changsha 410013, ChinaDepartment of Pediatrics, The Third Xiangya Hospital, Central South University, Changsha 410013, ChinaDepartment of Pediatrics, The Third Xiangya Hospital, Central South University, Changsha 410013, ChinaDepartment of Pediatrics, The Third Xiangya Hospital, Central South University, Changsha 410013, ChinaCardiovascular Department, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease, Guangzhou 510000, ChinaCardiovascular disease is a major cause of death worldwide. Inflammasome infiltration has been identified to play a central role in the pathological progression of certain cardiovascular diseases, such as vascular damage spanning atherosclerosis, aneurysm, or arteritis; ischemic heart disease; and other nonischemic heart diseases including diabetic cardiomyopathy, chronic heart failure, and hypertension- or virus-induced cardiac dysfunction. The NLRP3 inflammasome, a key participant in the innate immune response, requires both priming and activation signals for the initiation of inflammation. Piling evidence has revealed that the NLRP3 inflammasome could exert an inflammatory effect by inducing the secretion of proinflammatory cytokines (i.e., IL-1β, IL-18) or could cause pyroptosis, a novel programmed cell death process, in a caspase-1-dependent manner. The importance of the NLRP3 inflammasome in cardiac disease has been broadly investigated. In this review, we present the current knowledge regarding the function of NLRP in vascular disease, ischemic heart disease, and nonischemic heart disease and discuss the potential therapeutic options targeting the NLRP3 inflammasome.http://dx.doi.org/10.1155/2018/5702103
spellingShingle Wenyi Zhou
Chunyuan Chen
Zhiheng Chen
Lin Liu
Jie Jiang
Zhixiang Wu
Mingyi Zhao
Yanfang Chen
NLRP3: A Novel Mediator in Cardiovascular Disease
Journal of Immunology Research
title NLRP3: A Novel Mediator in Cardiovascular Disease
title_full NLRP3: A Novel Mediator in Cardiovascular Disease
title_fullStr NLRP3: A Novel Mediator in Cardiovascular Disease
title_full_unstemmed NLRP3: A Novel Mediator in Cardiovascular Disease
title_short NLRP3: A Novel Mediator in Cardiovascular Disease
title_sort nlrp3 a novel mediator in cardiovascular disease
url http://dx.doi.org/10.1155/2018/5702103
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