NLRP3炎性体在脑血管疾病病理中的作用及可能的治疗靶点。

IF 3.9 4区 医学 Q2 NEUROSCIENCES
Rongrong Bai, Yue Lang, Jie Shao, Yu Deng, Reyisha Refuhati, Li Cui
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引用次数: 36

摘要

脑血管疾病是涉及脑血流受损的病理状况,主要包括缺血性中风、颅内出血和蛛网膜下腔出血。核苷酸结合和寡聚化(NOD)结构域样受体(NLR)家族pyrin结构域(PYD)- 3 (NLRP3)炎症小体是一种蛋白质复合物,是免疫系统的重要组成部分。新的证据表明NLRP3炎性体在脑血管疾病中起重要作用。NLRP3炎性体在脑血管疾病发病机制中的作用仍是一个有趣的研究领域。本文首先综述了脑血管疾病的病理机制以及NLRP3炎性体加重动脉粥样硬化和脑血管疾病的病理机制。其次,我们概述了NLRP3炎性体参与加重或减轻脑血管疾病的信号通路。活化B细胞的活性氧(ROS)/核因子κ轻链增强子(NF-κB)、ROS/硫氧还蛋白相互作用蛋白(TXNIP)和嘌呤能受体-7 (P2X7R)信号通路可激活NLRP3炎性体;NLRP3炎性小体的激活可通过介导细胞凋亡和焦亡而加重脑血管疾病。据报道,自噬/线粒体自噬、核因子e2相关因子-2 (Nrf2)、干扰素(IFN)-β、sirtuin (SIRT)和磷酸肌肽3激酶(PI3K)/蛋白激酶B (AKT)通过抑制NLRP3炎性体激活来缓解脑血管疾病。最后,我们基于NLRP3炎性小体的两步活化,探索了NLRP3炎性小体的特异性抑制剂,可开发为治疗脑血管疾病的新药。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The Role of NLRP3 Inflammasome in Cerebrovascular Diseases Pathology and Possible Therapeutic Targets.

The Role of NLRP3 Inflammasome in Cerebrovascular Diseases Pathology and Possible Therapeutic Targets.

The Role of NLRP3 Inflammasome in Cerebrovascular Diseases Pathology and Possible Therapeutic Targets.

The Role of NLRP3 Inflammasome in Cerebrovascular Diseases Pathology and Possible Therapeutic Targets.

Cerebrovascular diseases are pathological conditions involving impaired blood flow in the brain, primarily including ischaemic stroke, intracranial haemorrhage, and subarachnoid haemorrhage. The nucleotide-binding and oligomerisation (NOD) domain-like receptor (NLR) family pyrin domain (PYD)-containing 3 (NLRP3) inflammasome is a protein complex and a vital component of the immune system. Emerging evidence has indicated that the NLRP3 inflammasome plays an important role in cerebrovascular diseases. The function of the NLRP3 inflammasome in the pathogenesis of cerebrovascular diseases remains an interesting field of research. In this review, we first summarised the pathological mechanism of cerebrovascular diseases and the pathological mechanism of the NLRP3 inflammasome in aggravating atherosclerosis and cerebrovascular diseases. Second, we outlined signalling pathways through which the NLRP3 inflammasome participates in aggravating or mitigating cerebrovascular diseases. Reactive oxygen species (ROS)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), ROS/thioredoxin-interacting protein (TXNIP) and purinergic receptor-7 (P2X7R) signalling pathways can activate the NLRP3 inflammasome; activation of the NLRP3 inflammasome can aggravate cerebrovascular diseases by mediating apoptosis and pyroptosis. Autophagy/mitochondrial autophagy, nuclear factor E2-related factor-2 (Nrf2), interferon (IFN)-β, sirtuin (SIRT), and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) reportedly alleviate cerebrovascular diseases by inhibiting NLRP3 inflammasome activation. Finally, we explored specific inhibitors of the NLRP3 inflammasome based on the two-step activation of the NLRP3 inflammasome, which can be developed as new drugs to treat cerebrovascular diseases.

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来源期刊
ASN NEURO
ASN NEURO NEUROSCIENCES-
CiteScore
7.70
自引率
4.30%
发文量
35
审稿时长
>12 weeks
期刊介绍: ASN NEURO is an open access, peer-reviewed journal uniquely positioned to provide investigators with the most recent advances across the breadth of the cellular and molecular neurosciences. The official journal of the American Society for Neurochemistry, ASN NEURO is dedicated to the promotion, support, and facilitation of communication among cellular and molecular neuroscientists of all specializations.
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