van Hout Gerardus P J, Bosch Lena
Department of Cardiology, Utrecht University Medical Center, Utrecht, The Netherlands.
Department of Experimental Cardiology, Utrecht University Medical Center, Utrecht, The Netherlands.
Exp Suppl. 2018;108:9-40. doi: 10.1007/978-3-319-89390-7_2.
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.
心血管疾病（CVD）是全球头号死因。构成CVD领域的各种疾病实体的发病机制复杂且具有多因素性。炎症在这些复杂病因中起着核心作用。炎性小体是由CVD（如动脉粥样硬化和心肌梗死（MI））中存在的危险相关分子模式（DAMP）激活的细胞内蛋白质复合物。经过启动和激活的两步过程后，炎性小体负责促炎细胞因子白细胞介素-1β和白细胞介素-18的形成，诱导信号转导级联反应，导致强烈的免疫反应，最终导致疾病进展。在过去几年中，人们对CVD中的炎性小体越来越感兴趣。炎性小体激活被认为参与了各种疾病实体的发病机制，如动脉粥样硬化、MI和心力衰竭（HF）。干扰炎性小体介导的信号传导可以减轻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以及对CVD可能的临床意义的现有文献。
