The Inflammasomes in Cardiovascular Disease.

Gerardus P J van Hout, Lena Bosch
{"title":"The Inflammasomes in Cardiovascular Disease.","authors":"Gerardus P J van Hout,&nbsp;Lena Bosch","doi":"10.1007/978-3-319-89390-7_2","DOIUrl":null,"url":null,"abstract":"<p><p>Cardiovascular disease (CVD) is the number one cause of death worldwide. The pathogenesis of various disease entities that comprise the area of CVD is complex and multifactorial. Inflammation serves a central role in these complex aetiologies. The inflammasomes are intracellular protein complexes activated by danger-associated molecular patterns (DAMPs) present in CVD such as atherosclerosis and myocardial infarction (MI). After a two-step process of priming and activation, inflammasomes are responsible for the formation of pro-inflammatory cytokines interleukin-1β and interleukin-18, inducing a signal transduction cascade resulting in a strong immune response that culminates in disease progression. In the past few years, increased interest has been raised regarding the inflammasomes in CVD. Inflammasome activation is thought to be involved in the pathogenesis of various disease entities such as atherosclerosis, MI and heart failure (HF). Interference with inflammasome-mediated signalling could reduce inflammation and attenuate the severity of disease. In this chapter we provide an overview of the current literature available on the role of inflammasome inhibition as a therapeutic intervention and the possible clinical implications for CVD.</p>","PeriodicalId":36906,"journal":{"name":"Experientia supplementum (2012)","volume":"108 ","pages":"9-40"},"PeriodicalIF":0.0000,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-319-89390-7_2","citationCount":"21","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experientia supplementum (2012)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-3-319-89390-7_2","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 21

Abstract

Cardiovascular disease (CVD) is the number one cause of death worldwide. The pathogenesis of various disease entities that comprise the area of CVD is complex and multifactorial. Inflammation serves a central role in these complex aetiologies. The inflammasomes are intracellular protein complexes activated by danger-associated molecular patterns (DAMPs) present in CVD such as atherosclerosis and myocardial infarction (MI). After a two-step process of priming and activation, inflammasomes are responsible for the formation of pro-inflammatory cytokines interleukin-1β and interleukin-18, inducing a signal transduction cascade resulting in a strong immune response that culminates in disease progression. In the past few years, increased interest has been raised regarding the inflammasomes in CVD. Inflammasome activation is thought to be involved in the pathogenesis of various disease entities such as atherosclerosis, MI and heart failure (HF). Interference with inflammasome-mediated signalling could reduce inflammation and attenuate the severity of disease. In this chapter we provide an overview of the current literature available on the role of inflammasome inhibition as a therapeutic intervention and the possible clinical implications for CVD.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
心血管疾病中的炎性小体。
心血管疾病(CVD)是全球头号死因。构成心血管疾病领域的各种疾病实体的发病机制是复杂和多因素的。炎症在这些复杂的病因中起着核心作用。炎症小体是由危险相关分子模式(DAMPs)激活的细胞内蛋白复合物,存在于心血管疾病,如动脉粥样硬化和心肌梗死(MI)中。经过启动和激活两步过程后,炎性小体负责形成促炎细胞因子白介素-1β和白介素-18,诱导信号转导级联,导致强烈的免疫反应,最终导致疾病进展。在过去的几年中,人们对炎症小体在心血管疾病中的作用越来越感兴趣。炎性小体活化被认为参与多种疾病的发病机制,如动脉粥样硬化、心肌梗死和心力衰竭(HF)。干扰炎性小体介导的信号可以减少炎症并减轻疾病的严重程度。在本章中,我们概述了目前关于炎性小体抑制作为一种治疗干预措施的作用和可能的临床意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Experientia supplementum (2012)
Experientia supplementum (2012) Medicine-Medicine (all)
CiteScore
3.30
自引率
0.00%
发文量
24
期刊最新文献
Mechanics of Microsporidian Polar Tube Firing. The Function and Structure of the Microsporidia Polar Tube. Insights from C. elegans into Microsporidia Biology and Host-Pathogen Relationships. Monoclonal Antibodies to CTLA-4 with Focus on Ipilimumab. Tumor-Infiltrating Lymphocytes and Their Role in Solid Tumor Progression.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1