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非编码RNA作为炎症性肠病中炎性小体调节的关键参与者;重点关注长链非编码RNA。

Non-coding RNAs as a Critical Player in the Regulation of Inflammasome in Inflammatory Bowel Diseases; Emphasize on lncRNAs.

作者信息

Salim Abed Hussein, Oghenemaro Enwa Felix, Kubaev Aziz, Jeddoa Zuhair Mohammed Ali, S RenukaJyothi, Sharma Shilpa, Vashishth Raghav, Jabir Majid S, Jawad Sabrean Farhan, Zwamel Ahmed Hussein

机构信息

Department of Medical Laboratory Techniques, Al-Maarif University College, Al-Anbar, Ramadi, Iraq.

Department of Pharmaceutical Microbiology, Faculty of Pharmacy, Delta State University, Abraka, Delta State, Nigeria.

出版信息

Cell Biochem Biophys. 2025 Jun;83(2):1359-1374. doi: 10.1007/s12013-024-01585-2. Epub 2024 Oct 19.

DOI:10.1007/s12013-024-01585-2
PMID:39424765
Abstract

Inflammatory bowel disease (IBD) is an idiopathic disease caused by a dysregulated immune response to host intestinal microflora. A hyperactive inflammatory and immunological response in the gut has been shown to be one of the disease's long-term causes despite the complexity of the clinical pathology of IBD. The innate immune system activator known as human gut inflammasome is thought to be a significant underlying cause of pathology and is closely linked to the development of IBD. It is essential to comprehend the function of inflammasome activation in IBD to treat it effectively. Systemic inflammasome regulation may be a proper therapeutic and clinical strategy to manage IBD symptoms since inflammasomes may have a significant function in IBD. Non-coding RNAs (ncRNAs) are a type of RNA transcript that is incapable of encoding proteins or peptides. In IBD, inflammation develops and worsens as a result of its imbalance. Culminating evidence has been shown that ncRNAs, and particularly long non-coding RNAs (lncRNAs), may play a role in the regulation of NLR family pyrin domain containing 3 (NLRP3) inflammasome activation in IBD. The relationship between IBD and the gut inflammasome, as well as current developments in IBD research and treatment approaches, have been the main topics of this review. We have covered inflammasomes and their constituents, results from in vivo research, inflammasome inhibitors, and advancements in inflammasome-targeted therapeutics for IBD.

摘要

炎症性肠病(IBD)是一种由对宿主肠道微生物群的免疫反应失调引起的特发性疾病。尽管IBD临床病理学复杂,但肠道中过度活跃的炎症和免疫反应已被证明是该疾病的长期病因之一。被称为人类肠道炎性小体的先天免疫系统激活剂被认为是病理的一个重要潜在原因,并且与IBD的发展密切相关。有效治疗IBD必须了解炎性小体激活在其中的作用。由于炎性小体可能在IBD中起重要作用,全身炎性小体调节可能是管理IBD症状的一种合适的治疗和临床策略。非编码RNA(ncRNA)是一种无法编码蛋白质或肽的RNA转录本。在IBD中,炎症因其失衡而发展和恶化。越来越多的证据表明,ncRNA,尤其是长链非编码RNA(lncRNA),可能在IBD中调节含NLR家族pyrin结构域3(NLRP3)炎性小体的激活中发挥作用。IBD与肠道炎性小体之间的关系,以及IBD研究和治疗方法的当前进展,一直是本综述的主要主题。我们涵盖了炎性小体及其成分、体内研究结果、炎性小体抑制剂以及针对IBD的炎性小体靶向治疗的进展。

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本文引用的文献

1
Role of long non-coding RNA in inflammatory bowel disease.长链非编码 RNA 在炎症性肠病中的作用。
Front Immunol. 2024 Jun 4;15:1406538. doi: 10.3389/fimmu.2024.1406538. eCollection 2024.
2
Transcription suppression of GABARAP mediated by lncRNA XIST-EZH2 interaction triggers caspase-11-dependent inflammatory injury in ulcerative colitis.长链非编码 RNA XIST-EZH2 相互作用介导的 GABARAP 转录抑制触发溃疡性结肠炎中 caspase-11 依赖性炎症损伤。
Immunobiology. 2024 May;229(3):152796. doi: 10.1016/j.imbio.2024.152796. Epub 2024 Mar 6.
3
METTL3-deficiency m6A-dependently degrades MALAT1 to suppress NLRP3-mediated pyroptotic cell death and inflammation in Mycobacterium tuberculosis (H37Ra strain)-infected mouse macrophages.
METTL3 缺乏依赖性地降解 MALAT1 以抑制分枝杆菌(H37Ra 株)感染的小鼠巨噬细胞中 NLRP3 介导热激细胞死亡和炎症。
Tuberculosis (Edinb). 2024 May;146:102502. doi: 10.1016/j.tube.2024.102502. Epub 2024 Mar 4.
4
LncRNA MSC-AS1 regulates SNIP1 SUMOylation-mediated EMT by binding to SENP1 to promote intestinal fibrosis in Crohn's disease.长链非编码 RNA MSC-AS1 通过与 SENP1 结合调节 SNIP1 的 SUMO 化介导的 EMT 来促进克罗恩病中的肠道纤维化。
Int J Biol Macromol. 2024 Mar;262(Pt 1):129921. doi: 10.1016/j.ijbiomac.2024.129921. Epub 2024 Feb 1.
5
KCNN4 links PIEZO-dependent mechanotransduction to NLRP3 inflammasome activation.KCNN4 将 PIEZO 依赖性机械转导与 NLRP3 炎性小体激活联系起来。
Sci Immunol. 2023 Dec 22;8(90):eadf4699. doi: 10.1126/sciimmunol.adf4699.
6
NAIP/NLRC4 inflammasome participates in macrophage responses to by a mechanism that relies on cathepsin-dependent caspase-1 cleavage.NAIP/NLRC4 炎性小体通过依赖组织蛋白酶依赖的半胱天冬酶-1 切割的机制参与巨噬细胞对 的反应。
Front Immunol. 2023 Dec 6;14:1282856. doi: 10.3389/fimmu.2023.1282856. eCollection 2023.
7
LncRNA Instigates Vascular Inflammation to Aggravate Atherosclerosis.长链非编码RNA引发血管炎症以加重动脉粥样硬化。
Circ Res. 2024 Jan 5;134(1):60-80. doi: 10.1161/CIRCRESAHA.122.322360. Epub 2023 Dec 12.
8
LncRNA GAS5 downregulates NLRP3 inflammasome activation-mediated pyroptosis in sepsis-induced myocardial injury by targeting SIRT3/AMPKα.长链非编码RNA GAS5通过靶向沉默调节蛋白3/腺苷酸活化蛋白激酶α下调脓毒症诱导的心肌损伤中NLRP3炎性小体激活介导的细胞焦亡。
Heliyon. 2023 Nov 28;9(12):e22939. doi: 10.1016/j.heliyon.2023.e22939. eCollection 2023 Dec.
9
Chlorogenic acid protects against myocardial ischemia-reperfusion injury in mice by inhibiting Lnc Neat1/NLRP3 inflammasome-mediated pyroptosis.绿原酸通过抑制 Lnc Neat1/NLRP3 炎性小体介导的细胞焦亡保护小鼠心肌缺血再灌注损伤。
Sci Rep. 2023 Oct 18;13(1):17803. doi: 10.1038/s41598-023-45017-2.
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Inflamm Res. 2023 Sep;72(9):1839-1859. doi: 10.1007/s00011-023-01790-4. Epub 2023 Sep 19.