细胞器交响曲:核因子红系2相关因子2和核因子κ B在脑卒中病理生物学中的作用。

IF 5.9 2区 医学 Q2 CELL BIOLOGY
Neural Regeneration Research Pub Date : 2026-04-01 Epub Date: 2025-03-25 DOI:10.4103/NRR.NRR-D-24-01404
Ziliang Hu, Mingyue Zhao, Hangyu Shen, Liangzhe Wei, Jie Sun, Xiang Gao, Yi Huang
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引用次数: 0

摘要

脑卒中包括缺血性脑卒中和出血性脑卒中,前者是由脑供血阻断或减少引起的,后者包括脑出血和蛛网膜下腔出血,以脑内出血为特征。中风是一种危及生命的脑血管疾病,具有复杂的病理生理机制,包括氧化应激、炎症、线粒体功能障碍和神经元损伤。关键转录因子,如核因子红系2相关因子2和核因子κ B在脑卒中的进展中起核心作用。核因子红系2相关因子2对细胞氧化还原状态的变化很敏感,在保护细胞免受氧化损伤、炎症反应和细胞毒性物质的影响方面起着至关重要的作用。它通过影响线粒体功能、内质网应激和溶酶体活性,调节代谢途径和细胞因子表达,在脑卒中后神经保护和修复中发挥重要作用。相反,核因子- kappab与线粒体功能障碍、活性氧的产生、氧化应激加剧和炎症密切相关。核因子κ b通过调节细胞粘附分子和炎症介质参与脑卒中后的神经元损伤、凋亡和免疫反应。这些通路之间的相互作用,可能涉及各种细胞器之间的串扰,显著影响中风的病理生理。单细胞测序和空间转录组学的进步极大地提高了我们对中风发病机制的理解,并为开发靶向、个体化、细胞类型特异性治疗提供了新的机会。在这篇综述中,我们讨论了核因子-红细胞2相关因子2和核因子- κ B参与缺血性和出血性卒中的机制,重点讨论了它们在氧化应激、炎症和神经保护中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Organelle symphony: Nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B in stroke pathobiology.

Strokes include both ischemic stroke, which is mediated by a blockade or reduction in the blood supply to the brain, and hemorrhagic stroke, which comprises intracerebral hemorrhage and subarachnoid hemorrhage and is characterized by bleeding within the brain. Stroke is a life-threatening cerebrovascular condition characterized by intricate pathophysiological mechanisms, including oxidative stress, inflammation, mitochondrial dysfunction, and neuronal injury. Critical transcription factors, such as nuclear factor erythroid 2-related factor 2 and nuclear factor kappa B, play central roles in the progression of stroke. Nuclear factor erythroid 2-related factor 2 is sensitive to changes in the cellular redox status and is crucial in protecting cells against oxidative damage, inflammatory responses, and cytotoxic agents. It plays a significant role in post-stroke neuroprotection and repair by influencing mitochondrial function, endoplasmic reticulum stress, and lysosomal activity and regulating metabolic pathways and cytokine expression. Conversely, nuclear factor-kappaB is closely associated with mitochondrial dysfunction, the generation of reactive oxygen species, oxidative stress exacerbation, and inflammation. Nuclear factor-kappaB contributes to neuronal injury, apoptosis, and immune responses following stroke by modulating cell adhesion molecules and inflammatory mediators. The interplay between these pathways, potentially involving crosstalk among various organelles, significantly influences stroke pathophysiology. Advancements in single-cell sequencing and spatial transcriptomics have greatly improved our understanding of stroke pathogenesis and offer new opportunities for the development of targeted, individualized, cell type-specific treatments. In this review, we discuss the mechanisms underlying the involvement of nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B in both ischemic and hemorrhagic stroke, with an emphasis on their roles in oxidative stress, inflammation, and neuroprotection.

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来源期刊
Neural Regeneration Research
Neural Regeneration Research CELL BIOLOGY-NEUROSCIENCES
CiteScore
8.00
自引率
9.80%
发文量
515
审稿时长
1.0 months
期刊介绍: Neural Regeneration Research (NRR) is the Open Access journal specializing in neural regeneration and indexed by SCI-E and PubMed. The journal is committed to publishing articles on basic pathobiology of injury, repair and protection to the nervous system, while considering preclinical and clinical trials targeted at improving traumatically injuried patients and patients with neurodegenerative diseases.
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