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Review
. 2018 Apr 8:2018:5702103.
doi: 10.1155/2018/5702103. eCollection 2018.

NLRP3: A Novel Mediator in Cardiovascular Disease

Wenyi Zhou  1   2 , Chunyuan Chen  3 , Zhiheng Chen  3 , Lin Liu  3 , Jie Jiang  3 , Zhixiang Wu  3 , Mingyi Zhao  3 , Yanfang Chen  1   4
Affiliations
Review

NLRP3: A Novel Mediator in Cardiovascular Disease

Wenyi Zhou et al. J Immunol Res. .

Abstract

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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Figures

Figure 1
Figure 1
Overall scheme of NLRP3 inflammasome activation.
See this image and copyright information in PMC

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