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多发性硬化症:NLRP3炎性小体、gasdermin D与治疗方法

Multiple sclerosis: the NLRP3 inflammasome, gasdermin D, and therapeutics.

作者信息

Brint Amie, Greene Seth, Fennig-Victor Alyssa R, Wang Shanzhi

机构信息

Chemistry Department, University of Arkansas at Little Rock, Little Rock, AR, USA.

College of Medicine and Graduate School, University of Arkansas for Medical Sciences, Little Rock, AR, USA.

出版信息

Ann Transl Med. 2024 Aug 1;12(4):62. doi: 10.21037/atm-23-1960. Epub 2024 Jun 5.

Abstract

Multiple sclerosis (MS) stands as a chronic inflammatory disease characterized by its neurodegenerative impacts on the central nervous system. The complexity of MS and the significant challenges it poses to patients have made the exploration of effective treatments a crucial area of research. Among the various mechanisms under investigation, the role of inflammation in MS progression is of particular interest. Inflammatory responses within the body are regulated by various cellular mechanisms, one of which involves the nucleotide-binding oligomerization domain (NOD)-, leucine-rich repeat (LRR)-, and pyrin domains (PYD)-containing protein 3 (NLRP3). NLRP3 acts as a sensor within cells, playing a pivotal role in controlling the inflammatory response. Its activation is a critical step leading to the assembly of the NLRP3 inflammasome complex, a process that has profound implications for inflammatory diseases like MS. The NLRP3 inflammasome's activation is intricately linked to the subsequent activation of caspase 1 and gasdermin D (GsdmD), signaling pathways that are central to the inflammatory process. GsdmD, a prominent member of the Gasdermin protein family, is particularly noteworthy for its role in pyroptotic cell death, a form of programmed cell death that is distinct from apoptosis and is characterized by its inflammatory nature. This pathway's activation contributes significantly to the pathology of MS by exacerbating inflammatory responses within the nervous system. Given the detrimental effects of unregulated inflammation in MS, therapeutics targeting these inflammatory processes offer a promising avenue for alleviating the symptoms experienced by patients. This review delves into the intricacies of the pyroptotic pathways, highlighting how the formation of the NLRP3 inflammasome induces such pathways and the potential intervention points for therapeutic agents. By inhibiting key steps within these pathways, it is possible to mitigate the inflammatory response, thereby offering relief to those suffering from MS. Understanding these mechanisms not only sheds light on the pathophysiology of MS but also paves the way for the development of novel therapeutic strategies aimed at controlling the disease's progression through the modulation of the body's inflammatory response.

摘要

多发性硬化症(MS)是一种慢性炎症性疾病,其特征在于对中枢神经系统产生神经退行性影响。MS的复杂性及其给患者带来的重大挑战使得探索有效的治疗方法成为一个关键的研究领域。在正在研究的各种机制中,炎症在MS进展中的作用尤为令人关注。体内的炎症反应由多种细胞机制调节,其中之一涉及含核苷酸结合寡聚化结构域(NOD)、富含亮氨酸重复序列(LRR)和吡啉结构域(PYD)的蛋白3(NLRP3)。NLRP3在细胞内充当传感器,在控制炎症反应中起关键作用。其激活是导致NLRP3炎性小体复合物组装的关键步骤,这一过程对MS等炎症性疾病具有深远影响。NLRP3炎性小体的激活与半胱天冬酶1和gasdermin D(GsdmD)的后续激活密切相关,这些信号通路是炎症过程的核心。GsdmD是Gasdermin蛋白家族的重要成员,因其在焦亡性细胞死亡中的作用而特别值得关注,焦亡性细胞死亡是一种程序性细胞死亡形式,与细胞凋亡不同,其特点是具有炎症性质。该途径的激活通过加剧神经系统内的炎症反应,对MS的病理过程有显著贡献。鉴于MS中不受控制的炎症的有害影响,针对这些炎症过程的治疗方法为减轻患者的症状提供了一条有前景的途径。本综述深入探讨了焦亡途径的复杂性,强调了NLRP3炎性小体的形成如何诱导这些途径以及治疗药物的潜在干预点。通过抑制这些途径中的关键步骤,可以减轻炎症反应,从而为MS患者提供缓解。了解这些机制不仅有助于阐明MS的病理生理学,还为开发旨在通过调节身体的炎症反应来控制疾病进展的新型治疗策略铺平了道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/716f/11304424/f3db377a8aa7/atm-12-04-62-f1.jpg

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