Role of the Inflammasome in Liver Disease.

IF 28.4 1区医学 Q1 PATHOLOGY

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2022-01-24 DOI:10.1146/annurev-pathmechdis-032521-102529

Marcelle de Carvalho Ribeiro, Gyongyi Szabo

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引用次数: 62

Abstract

The involvement of inflammasomes in the proinflammatory response observed in chronic liver diseases, such as alcohol-associated liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD), is widely recognized. Although there are different types of inflammasomes, most studies to date have given attention to NLRP3 (nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3) in the pathogenesis of ALD, NAFLD/nonalcoholic steatohepatitis, and fibrosis. Canonical inflammasomes are intracellular multiprotein complexes that are assembled after the sensing of danger signals and activate caspase-1, which matures interleukin (IL)-1β, IL-18, and IL-37 and also induces a form of cell death called pyroptosis. Noncanonical inflammasomes activate caspase-11 to induce pyroptosis. We discuss the different types of inflammasomes involved in liver diseases with a focus on (a) signals and mechanisms of inflammasome activation, (b) the role of different types of inflammasomes and their products in the pathogenesis of liver diseases, and (c) potential therapeutic strategies targeting components of the inflammasomes or cytokines produced upon inflammasome activation.

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炎性体在肝脏疾病中的作用。

炎症小体参与慢性肝病(如酒精相关性肝病(ALD)和非酒精性脂肪性肝病(NAFLD))中观察到的促炎反应已被广泛认可。尽管存在不同类型的炎症小体，但迄今为止大多数研究都关注NLRP3(核苷酸结合寡聚化结构域样受体家族，pyrin结构域3)在ALD、NAFLD/非酒精性脂肪性肝炎和纤维化发病机制中的作用。典型炎症小体是细胞内的多蛋白复合物，在感知危险信号后组装并激活caspase-1, caspase-1使白细胞介素(IL)-1β， IL-18和IL-37成熟，并诱导一种称为焦亡的细胞死亡形式。非典型炎性小体激活caspase-11诱导焦亡。我们讨论了与肝脏疾病相关的不同类型的炎症小体，重点关注(a)炎症小体激活的信号和机制，(b)不同类型的炎症小体及其产物在肝脏疾病发病机制中的作用，以及(c)针对炎症小体的成分或炎症小体激活时产生的细胞因子的潜在治疗策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Annual Review of Pathology-Mechanisms of Disease 医学-病理学

CiteScore

62.60

自引率

0.00%

发文量

期刊介绍： The Annual Review of Pathology: Mechanisms of Disease is a scholarly journal that has been published since 2006. Its primary focus is to provide a comprehensive overview of recent advancements in our knowledge of the causes and development of significant human diseases. The journal places particular emphasis on exploring the current and evolving concepts of disease pathogenesis, as well as the molecular genetic and morphological changes associated with various diseases. Additionally, the journal addresses the clinical significance of these findings. In order to increase accessibility and promote the broad dissemination of research, the current volume of the journal has transitioned from a gated subscription model to an open access format. This change has been made possible through the Annual Reviews' Subscribe to Open program, which allows all articles published in this volume to be freely accessible to readers. As part of this transition, all articles in the journal are published under a Creative Commons Attribution (CC BY) license, which encourages open sharing and use of the research.