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炎症小体病中的微小RNA

MicroRNAs in inflammasomopathies.

作者信息

Saad Norma, Duroux-Richard Isabelle, Touitou Isabelle, Jeziorski Eric, Apparailly Florence

机构信息

Institute for Regenerative Medicine and Biotherapy, INSERM, U1183, University of Montpellier, Montpellier, France.

Institute for Regenerative Medicine and Biotherapy, INSERM, U1183, University of Montpellier, Montpellier, France; Department of Molecular genetics, Medical Genetics of Rare and Autoinflammatory disease unit, Montpellier University Hospital, Montpellier, France; Centre de référence des maladies autoinflammatoires et des amyloses d'origine inflammatoire, CeRéMAIA, Montpellier University Hospital, Montpellier, France.

出版信息

Immunol Lett. 2023 Apr-May;256-257:48-54. doi: 10.1016/j.imlet.2023.04.001. Epub 2023 Apr 5.

DOI:10.1016/j.imlet.2023.04.001
PMID:37023968
Abstract

microRNAs (miRNAs) are small non-coding RNA sequences that negatively regulate the expression of protein-encoding genes at the post-transcriptional level. They play a role in the regulation of inflammatory responses by controlling the proliferation and activation of immune cells and their expression is disrupted in several immune-mediated inflammatory disorders. Among these, autoinflammatory diseases (AID) are a group of rare hereditary disorders caused by abnormal activation of the innate immune system and characterized by recurrent fevers. Major groups of AID are inflammasomopathies, which are associated with hereditary defects in the activation of inflammasomes, cytosolic multiprotein signaling complexes regulating IL-1 family cytokine maturation and pyroptosis. The study of the role of miRNAs in AID is only recently emerging and remains scarce in inflammasomopathies. In this review, we describe the AID and inflammasomopathies, and the current knowledge on the role of miRNAs in disease processes.

摘要

微小RNA(miRNA)是小的非编码RNA序列,它们在转录后水平上负向调节蛋白质编码基因的表达。它们通过控制免疫细胞的增殖和活化在炎症反应调节中发挥作用,并且其表达在几种免疫介导的炎症性疾病中受到破坏。其中,自身炎症性疾病(AID)是一组由先天免疫系统异常激活引起的罕见遗传性疾病,其特征为反复发热。AID的主要类型是炎性小体病,它与炎性小体激活的遗传性缺陷有关,炎性小体是调节IL-1家族细胞因子成熟和细胞焦亡的胞质多蛋白信号复合物。miRNA在AID中的作用研究最近才刚刚兴起,在炎性小体病方面仍然很少。在这篇综述中,我们描述了AID和炎性小体病,以及目前关于miRNA在疾病过程中作用的知识。

相似文献

1
MicroRNAs in inflammasomopathies.炎症小体病中的微小RNA
Immunol Lett. 2023 Apr-May;256-257:48-54. doi: 10.1016/j.imlet.2023.04.001. Epub 2023 Apr 5.
2
An Update on Autoinflammatory Diseases: Inflammasomopathies.自身炎症性疾病的最新进展:炎症小体病。
Curr Rheumatol Rep. 2018 May 30;20(7):40. doi: 10.1007/s11926-018-0750-4.
3
Rare hereditary autoinflammatory disorders: towards an understanding of critical in vivo inflammatory pathways.罕见遗传性自身炎症性疾病:深入理解关键的体内炎症通路。
J Dermatol Sci. 2012 Jun;66(3):183-9. doi: 10.1016/j.jdermsci.2012.01.004. Epub 2012 Jan 18.
4
[Diagnosis and Clinical Examination of Autoinflammatory Syndrome].[自身炎症性综合征的诊断与临床检查]
Rinsho Byori. 2015 May;63(5):598-604.
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Deregulated inflammasome signaling in disease.失调的炎症小体信号在疾病中的作用。
Immunol Rev. 2011 Sep;243(1):163-73. doi: 10.1111/j.1600-065X.2011.01042.x.
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Inflammasomes and dermatology.炎性小体与皮肤病学
An Bras Dermatol. 2016 Sep-Oct;91(5):566-578. doi: 10.1590/abd1806-4841.20165577.
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[Pathogenesis and Clinical Examination of Autoinflammatory Syndrome].[自身炎症综合征的发病机制与临床检查]
Rinsho Byori. 2015 Oct;63(10):1207-12.
8
Activation and Pharmacological Regulation of Inflammasomes.炎症小体的激活与药理学调控
Biomolecules. 2022 Jul 20;12(7):1005. doi: 10.3390/biom12071005.
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Genetic and epigenetic dysregulation of innate immune mechanisms in autoinflammatory diseases.自身炎症性疾病中固有免疫机制的遗传和表观遗传失调。
FEBS J. 2024 Oct;291(20):4414-4432. doi: 10.1111/febs.17116. Epub 2024 Mar 12.
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Inflammasome and cytokine blocking strategies in autoinflammatory disorders.自身炎症性疾病中炎性小体和细胞因子阻断策略。
Clin Immunol. 2013 Jun;147(3):242-75. doi: 10.1016/j.clim.2013.04.008. Epub 2013 Apr 19.

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ACS Pharmacol Transl Sci. 2025 Apr 30;8(5):1205-1226. doi: 10.1021/acsptsci.4c00681. eCollection 2025 May 9.
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MiR-146a Reduces Inflammation in Experimental Pancreatitis via the TRAF6-NF-κB Signaling Pathway in Mice.微小RNA-146a通过小鼠体内TRAF6-NF-κB信号通路减轻实验性胰腺炎中的炎症反应。
Immun Inflamm Dis. 2025 Mar;13(3):e70163. doi: 10.1002/iid3.70163.
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Reframing the link between metabolism and NLRP3 inflammasome: therapeutic opportunities.重新构建代谢与 NLRP3 炎性小体之间的联系:治疗机会。
Front Immunol. 2023 Jul 20;14:1232629. doi: 10.3389/fimmu.2023.1232629. eCollection 2023.