Review: Progress of the NLRP3 inflammasome in tumours and perspectives for cholangiocarcinoma.

IF 8.2 2区 生物学 Q1 CELL BIOLOGY
Zhaoqin Zhuo, Yuwei Xie, Hao Zou, Bin Tan, Qian Dong, Bingzi Dong, Chengzhan Zhu
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引用次数: 0

Abstract

The NLRP3 inflammasome is a multi-protein complex that mediates intense inflammatory responses. Its activation and function are influenced by various factors, including the recognition of pathogen-associated molecular patterns and damage-associated molecular patterns, cellular stress responses, and metabolic disorders. Recent research has extensively studied the role of the NLRP3 inflammasome in tumors. Findings indicate that tumor cells and macrophages can regulate the activation of the NLRP3 inflammasome, promoting tumor development and progression. Conversely, the NLRP3 inflammasome can also exhibit anti-tumor effects through immune cells, such as dendritic cells. This has led to the development of treatment strategies, creating a comprehensive treatment system that includes sensitizers for radiotherapy and chemotherapy, inhibitors of the NLRP3 inflammasome pathway, and direct targeting of the NLRP3 inflammasome.Cholangiocarcinoma is a highly invasive and heterogeneous malignant tumor. Due to its non-specific symptoms, patients often present with advanced stages of the disease, and the mortality rate continues to rise annually. A deeper exploration of the mechanisms underlying cholangiocarcinoma's occurrence and development is essential for improving diagnosis and treatment strategies. The application of multi-omics analysis in cholangiocarcinoma research lays a foundation for understanding its pathogenesis and potential treatments. This article systematically reviews the latest advancements in NLRP3 inflammasome research, including its regulatory mechanisms, role in promoting tumor development, and effects in anti-tumor immunotherapy. Additionally, by summarizing the mechanisms involved in cholangiocarcinoma, we hypothesize that the NLRP3 inflammasome may play a significant role in the occurrence and development of cholangiocarcinoma. Therefore, we conduct a multi-angle analysis of the potential relationship between the two and propose a hypothesis model. The goal of this article is to explore the role of the NLRP3 inflammasome in tumors and its potential relationship with cholangiocarcinoma, offering new insights for research on the link between cholangiocarcinoma-related inflammation and the disease itself.

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综述:NLRP3炎性体在肿瘤中的研究进展及胆管癌的研究前景。
NLRP3炎性小体是一种介导强烈炎症反应的多蛋白复合物。它的激活和功能受到多种因素的影响,包括病原体相关分子模式和损伤相关分子模式的识别、细胞应激反应和代谢紊乱。最近的研究广泛研究了NLRP3炎性体在肿瘤中的作用。研究结果表明,肿瘤细胞和巨噬细胞可调节NLRP3炎性体的激活,促进肿瘤的发生发展。相反,NLRP3炎性体也可以通过免疫细胞(如树突状细胞)表现出抗肿瘤作用。这导致了治疗策略的发展,创造了一个综合的治疗系统,包括放疗和化疗的增敏剂,NLRP3炎症小体途径的抑制剂,以及NLRP3炎症小体的直接靶向。胆管癌是一种高度侵袭性、异质性的恶性肿瘤。由于其非特异性症状,患者往往表现为疾病的晚期,死亡率每年持续上升。深入探讨胆管癌发生发展的机制对于提高诊断和治疗策略至关重要。多组学分析在胆管癌研究中的应用为了解其发病机制和潜在的治疗方法奠定了基础。本文系统综述了NLRP3炎性小体的最新研究进展,包括其调控机制、促进肿瘤发展的作用以及在抗肿瘤免疫治疗中的作用。此外,通过对胆管癌相关机制的总结,我们推测NLRP3炎性体可能在胆管癌的发生发展中发挥重要作用。因此,我们对两者之间的潜在关系进行多角度分析,并提出假设模型。本文旨在探讨NLRP3炎性小体在肿瘤中的作用及其与胆管癌的潜在关系,为研究胆管癌相关炎症与疾病本身的关系提供新的见解。
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
CiteScore
11.00
自引率
0.00%
发文量
180
期刊介绍: Cell Communication and Signaling (CCS) is a peer-reviewed, open-access scientific journal that focuses on cellular signaling pathways in both normal and pathological conditions. It publishes original research, reviews, and commentaries, welcoming studies that utilize molecular, morphological, biochemical, structural, and cell biology approaches. CCS also encourages interdisciplinary work and innovative models, including in silico, in vitro, and in vivo approaches, to facilitate investigations of cell signaling pathways, networks, and behavior. Starting from January 2019, CCS is proud to announce its affiliation with the International Cell Death Society. The journal now encourages submissions covering all aspects of cell death, including apoptotic and non-apoptotic mechanisms, cell death in model systems, autophagy, clearance of dying cells, and the immunological and pathological consequences of dying cells in the tissue microenvironment.
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