Fan Hua, Fu Qizhi, Du Ganqin, Qin Ling, Shi Xiaofei, Wang Dongmei, Yang Yanhui
Office of Research & Innovation, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Department of Intensive Medicine, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
CNS Neurosci Ther. 2024 Dec;30(12):e70135. doi: 10.1111/cns.70135.
This review delves into the intricate relationship between NLR inflammasomes, particularly the NLRP3 inflammasome, and the immune-mediated neurodegenerative disease, multiple sclerosis (MS). While the precise etiology of MS remains elusive, compelling research underscores the pivotal role of the immune response in disease progression. Notably, recent investigations highlight the significant involvement of NLRP3 inflammasomes in various autoimmune diseases, prompting an in-depth exploration of their impact on MS.
The review focuses on elucidating the activation mechanism of NLRP3 inflammasomes within microglia/macrophages (MG/MФ), examining how this activation promotes an inflammatory response that exacerbates neuronal damage in MS. A comprehensive analysis of existing literature and research findings forms the basis for understanding the intricate interplay between NLRP3 inflammasomes and MS pathogenesis.
Synthesizing current research, the review provides insight into the pivotal role played by NLR inflammasomes, specifically NLRP3, in MS. Emphasis is placed on the inflammatory response orchestrated by activated MG/MФ, elucidating the cascade that perpetuates neuronal damage in the disease.
This review concludes by consolidating key findings and offering a nuanced perspective on the role of NLRP3 inflammasomes in MS pathogenesis. The detailed exploration of the activation process within MG/MФ provides a foundation for understanding the disease's underlying mechanisms. Furthermore, the review sets the stage for potential therapeutic strategies targeting NLRP3 inflammasomes in the pursuit of MS treatment.
本综述深入探讨了NLR炎性小体，特别是NLRP3炎性小体与免疫介导的神经退行性疾病——多发性硬化症（MS）之间的复杂关系。虽然MS的确切病因仍不明确，但有力的研究强调了免疫反应在疾病进展中的关键作用。值得注意的是，最近的研究突出了NLRP3炎性小体在各种自身免疫性疾病中的重要参与，促使人们深入探究其对MS的影响。
本综述着重阐明小胶质细胞/巨噬细胞（MG/MФ）内NLRP3炎性小体的激活机制，研究这种激活如何促进炎症反应，进而加剧MS中的神经元损伤。对现有文献和研究结果的全面分析构成了理解NLRP3炎性小体与MS发病机制之间复杂相互作用关系的基础。
综合当前研究，本综述深入探讨了NLR炎性小体，特别是NLRP3在MS中所起的关键作用。重点关注激活的MG/MФ所引发的炎症反应，阐明了在该疾病中使神经元损伤持续存在的级联反应。
本综述通过整合关键发现，对NLRP3炎性小体在MS发病机制中的作用提供了细致入微洞察。对MG/MФ内激活过程的详细探索为理解该疾病的潜在机制奠定了基础。此外，本综述为在MS治疗中针对NLRP3炎性小体的潜在治疗策略搭建了框架。
