Lu Yujia, Cheng Lin, Xiong Yinyi, Huang Chunyan, Liu Ziying, Shen Chunxiao, Wang Huaying, Qiu Yuemin, Yang Seung Bum, Wu Moxin, Zhang Xiaorong
Department of Pathology, Clinical Medical School of Jiujiang University, Jiujiang, Jiangxi, China.
Jiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, China.
CNS Neurosci Ther. 2025 May;31(5):e70403. doi: 10.1111/cns.70403.
Vascular dementia, the second most common type of dementia globally after Alzheimer's disease, is associated with neuroinflammation. Activation of the NLRP3 inflammasome, an important pattern recognition receptor in human innate immunity, plays a key role in the pathogenesis of vascular dementia.
The NLRP3 inflammasome pathway destroys neuronal cells primarily through the production of IL-18 and IL-1β. Moreover, it exacerbates vascular dementia by producing IL-18, IL-1β, and the N-terminal fragment of GSDMD, which also contributes to neuronal cell death. Thus, blocking the NLRP3 inflammasome pathway presents a new therapeutic strategy for treating vascular dementia, thereby delaying or curing the disease more effectively and mitigating adverse effects.
This review explores the role and mechanisms of the NLRP3 inflammasome in vascular dementia, summarizing current research and therapeutic strategies. Investigating the activation of the NLRP3 inflammasome can reveal the pathogenesis of vascular dementia from a new perspective and propose innovative preventive and treatment strategies.
血管性痴呆是全球仅次于阿尔茨海默病的第二常见痴呆类型，与神经炎症相关。NLRP3炎性小体是人类固有免疫中一种重要的模式识别受体，其激活在血管性痴呆的发病机制中起关键作用。
NLRP3炎性小体途径主要通过产生IL-18和IL-1β来破坏神经元细胞。此外，它通过产生IL-18、IL-1β和GSDMD的N端片段加剧血管性痴呆，这也导致神经元细胞死亡。因此，阻断NLRP3炎性小体途径为治疗血管性痴呆提供了一种新的治疗策略，从而更有效地延缓或治愈该疾病并减轻不良反应。
本综述探讨了NLRP3炎性小体在血管性痴呆中的作用和机制，总结了当前的研究和治疗策略。研究NLRP3炎性小体的激活可以从新的角度揭示血管性痴呆的发病机制，并提出创新的预防和治疗策略。
