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Regulatory Mechanisms of the NLRP3 Inflammasome, a Novel Immune-Inflammatory Marker in Cardiovascular Diseases.

The nod-like receptor family pyrin domain containing 3 (NLRP3) is currently the most widely studied inflammasome and has become a hot topic of recent research. As a macromolecular complex, the NLRP3 inflammasome is activated to produce downstream factors, including caspase-1, IL-1β, and IL-18, which... Full description

Journal Title: Frontiers in immunology 2019, Vol.10, p.1592
Main Author: An, Na
Other Authors: Gao, Yonghong , Si, Zeyu , Zhang, Hanlai , Wang, Liqin , Tian, Chao , Yuan, Mengchen , Yang, Xinyu , Li, Xinye , Shang, Hongcai , Xiong, Xingjiang , Xing, Yanwei
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1664-3224 ; DOI: 1664-3224 ; DOI: 10.3389/fimmu.2019.01592
Link: http://search.proquest.com/docview/2266347732/?pq-origsite=primo
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title: Regulatory Mechanisms of the NLRP3 Inflammasome, a Novel Immune-Inflammatory Marker in Cardiovascular Diseases.
format: Article
creator:
  • An, Na
  • Gao, Yonghong
  • Si, Zeyu
  • Zhang, Hanlai
  • Wang, Liqin
  • Tian, Chao
  • Yuan, Mengchen
  • Yang, Xinyu
  • Li, Xinye
  • Shang, Hongcai
  • Xiong, Xingjiang
  • Xing, Yanwei
subjects:
  • Nlrp3 Inflammasome
  • Cardiovascular Diseases
  • Coronary Atherosclerosis
  • Immune-Inflammatory
  • Myocardial Ischemia/Reperfusion
ispartof: Frontiers in immunology, 2019, Vol.10, p.1592
description: The nod-like receptor family pyrin domain containing 3 (NLRP3) is currently the most widely studied inflammasome and has become a hot topic of recent research. As a macromolecular complex, the NLRP3 inflammasome is activated to produce downstream factors, including caspase-1, IL-1β, and IL-18, which then promote local inflammatory responses and induce pyroptosis, leading to unfavorable effects. A growing number of studies have examined the relationship between the NLRP3 inflammasome and cardiovascular diseases (CVDs). However, some studies have shown that the NLRP3 inflammasome is not involved in the occurrence of certain diseases. Therefore, identifying the mechanism of action of the NLRP3 inflammasome and its potential involvement in the pathological process of disease progression is of utmost importance. This review discusses the mechanisms of NLRP3 inflammasome activation and the relationship between the inflammasome and CVDs, including coronary atherosclerosis, myocardial ischemia/reperfusion, cardiomyopathies, and arrhythmia, as well as CVD-related treatments.
language: eng
source:
identifier: E-ISSN: 1664-3224 ; DOI: 1664-3224 ; DOI: 10.3389/fimmu.2019.01592
fulltext: fulltext
issn:
  • 16643224
  • 1664-3224
url: Link


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titleRegulatory Mechanisms of the NLRP3 Inflammasome, a Novel Immune-Inflammatory Marker in Cardiovascular Diseases.
creatorAn, Na ; Gao, Yonghong ; Si, Zeyu ; Zhang, Hanlai ; Wang, Liqin ; Tian, Chao ; Yuan, Mengchen ; Yang, Xinyu ; Li, Xinye ; Shang, Hongcai ; Xiong, Xingjiang ; Xing, Yanwei
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descriptionThe nod-like receptor family pyrin domain containing 3 (NLRP3) is currently the most widely studied inflammasome and has become a hot topic of recent research. As a macromolecular complex, the NLRP3 inflammasome is activated to produce downstream factors, including caspase-1, IL-1β, and IL-18, which then promote local inflammatory responses and induce pyroptosis, leading to unfavorable effects. A growing number of studies have examined the relationship between the NLRP3 inflammasome and cardiovascular diseases (CVDs). However, some studies have shown that the NLRP3 inflammasome is not involved in the occurrence of certain diseases. Therefore, identifying the mechanism of action of the NLRP3 inflammasome and its potential involvement in the pathological process of disease progression is of utmost importance. This review discusses the mechanisms of NLRP3 inflammasome activation and the relationship between the inflammasome and CVDs, including coronary atherosclerosis, myocardial ischemia/reperfusion, cardiomyopathies, and arrhythmia, as well as CVD-related treatments.
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