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中华肝脏外科手术学电子杂志

中华肝脏外科手术学电子杂志 ›› 2026, Vol. 15 ›› Issue (02) : 271 -277. doi: 10.3877/cma.j.issn.2095-3232.2026.02.020

综述

NLRP3炎症小体在非酒精性脂肪性肝病中的研究进展
张浩波1, 牛剑祥2,†()   
  1. 1　010000　呼和浩特，内蒙古医科大学
    2　010000　呼和浩特，内蒙古医科大学附属医院肝胆外科C区
  • 收稿日期:2025-10-11 出版日期:2026-04-10
  • 通信作者: 牛剑祥
  • 基金资助:
    国家自然科学基金(82473613); 内蒙古医科大学联合项目(YKD2023LH046)

Research progress in NLRP3 inflammosome in non-alcoholic fatty liver disease

Haobo Zhang1, Jianxiang Niu2,†()   

  1. 1 Inner Mongolia Medical University, Hohhot 010000, China
    2 Department of Hepatobiliary Surgery Section C, the Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010000, China
  • Received:2025-10-11 Published:2026-04-10
  • Corresponding author: Jianxiang Niu
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张浩波, 牛剑祥. NLRP3炎症小体在非酒精性脂肪性肝病中的研究进展[J/OL]. 中华肝脏外科手术学电子杂志, 2026, 15(02): 271-277.

Haobo Zhang, Jianxiang Niu. Research progress in NLRP3 inflammosome in non-alcoholic fatty liver disease[J/OL]. Chinese Journal of Hepatic Surgery(Electronic Edition), 2026, 15(02): 271-277.

非酒精性脂肪性肝病（NAFLD）作为全球最常见的慢性肝病。近年来研究揭示，核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）炎症小体作为先天免疫系统的核心调控节点，通过整合脂毒性、氧化应激及肠-肝轴紊乱信号，在NAFLD向非酒精性脂肪性肝炎及肝纤维化的进展中发挥关键作用。本综述系统总结了NLRP3炎症小体的分子结构、激活途径及其核心调控机制。此外，靶向NLRP3的小分子抑制剂、天然化合物及基因编辑技术已在临床前模型中展现出显著疗效，提示其作为NAFLD治疗新策略的潜力。然而，当前研究仍面临细胞异质性调控机制不清、时空动态性研究不足及临床转化瓶颈等挑战，未来需整合单细胞与空间组学技术，解析肝脏微环境中NLRP3的细胞特异性激活模式；结合多组学数据阐明代谢-炎症交互网络；并开发变构抑制剂或靶向递送系统以提高治疗特异性。通过跨学科技术融合与临床研究范式革新，NLRP3炎症小体靶向治疗有望为NAFLD患者提供精准且安全的干预方案，推动从基础研究向临床应用的跨越。

关键词: NLRP3炎症小体, 非酒精性脂肪性肝病, 氧化应激, 脂毒性, 基因编辑

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. Recent studies have revealed that nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) inflammasome, as the core regulatory node of innate immune system, play a key role in the progression from NAFLD to nonalcoholic steatohepatitis and liver fibrosis by integrating the signals of lipotoxicity, oxidative stress and gut-liver axis disorder. In this review, the molecular structure, activation pathway and core regulatory mechanisms of NLRP3 inflammosome were systematically summarized. In addition, small molecular inhibitors, natural compounds and gene editing technologies targeting NLRP3 have shown remarkable efficacy in preclinical models, suggesting its potential as a novel therapeutic strategy for NAFLD. However, current research still faces multiple challenges, such as unclear regulatory mechanism of cell heterogeneity, insufficient research on spatio-temporal dynamics and bottleneck of clinical translation. Subsequently, it is necessary to integrate single-cell and spatial genomics technologies to analyze the cell-specific activation mode of NLRP3 in liver microenvironment. The metabolic-inflammatory interaction network can be elucidated by combining multi-omics data. Allosteric inhibitors or targeted delivery systems can be developed to improve treatment specificity. Through interdisciplinary technological integration and clinical research innovation, NLRP3 inflammatosome-targeted therapy is expected to provide precise and safe intervention protocols for NAFLD patients and promote the translation from basic research to clinical application.

Key words: NLRP3 inflammasome, Non-alcoholic fatty liver disease, Oxidative stress, Lipotoxicity, Gene editing
图1 NLRP3炎症小体的结构域及通路分子模型[11] 注：a为胞内模式识别受体NLRP3的3个组成部分，包含N端的PYD、中央的NACHT结构域、C端的LRR结构域；PYD为氨基末端pyrin结构域，LRR为亮氨酸重复区，NACHT为核酸结合寡聚化结构域，FISNA为鱼类特异性NACHT相关结构域，NBD为核苷酸结合结构域，HD为螺旋结构域，WHD为翼螺旋结构域；b为ASC通过其PYD与NLRP3结合，并通过CARD招募pro-caspase-1，促使后者自剪切为活性形式caspase-1；ASC为凋亡相关斑点样蛋白，CARD为半胱天冬酶激活和募集结构域；c为NLRP3炎症体途径的通路分子级联反应模型；PAMPs/DAMPs导致NLRP3构象变化，使NLRP3与NIMA相关激酶7（NEK7）结合诱导形成NLRP3炎症小体盘状结构，并促使NLRP3 PYD形成丝状聚合体，该PYD丝状体通过成核作用招募ASC的PYD结构域形成ASC PYD丝状体，ASC的CARD随之聚集形成丝状结构，进而通过成核作用招募caspase-1的CARD结构域形成丝状体，caspase-1的酶催化结构域（p20/p10）发生二聚化并自我水解，从而激活酶活性，活化的caspase-1切割IL-1家族细胞因子前体产生成熟细胞因子，同时切割消皮素D(GSDMD)释放其活性N端片段，该片段在细胞膜上成孔，驱动细胞因子释放并引发细胞焦亡，caspase-1为半胱氨酸-天冬氨酸特异性蛋白酶-1
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