Iron in multiple sclerosis - from pathophysiology to disease progression - a narrative literature review.

IF 1.4 4区 医学 Q4 NEUROSCIENCES
Karolina Kłodnicka, Jacek Januszewski, Alicja Forma, Weronika Pająk, Barbara Teresińska, Jacek Baj
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Abstract

Multiple sclerosis (MS) is a chronic autoimmune illness characterized by demyelination and neurodegeneration, which causes physical disability and severe alterations in the neurological system, including gliosis and neuron loss. The disease primarily affects myelinated parts of the central nervous system (CNS), such as the optic nerves, cerebellum, brain stem, and spinal cord. T cells play an important role in MS pathogenesis by inducing demyelination, and risk factors include genetic predisposition, environmental effects, and lifestyle decisions. The prevalence of MS is rising, especially among women and the elderly population. Iron dysregulation is a critical element in MS pathogenesis, with excess iron causing neurodegeneration via ferroptosis and immune response modulation. Excess iron amplifies inflammation by triggering the activation of macrophages with inflammatory properties, and promoting microglial polarization toward the pro‑inflammatory phenotype. This causes increased oxidative stress, mitochondrial malfunction, and the release of reactive oxygen species, which harm neurons. Furthermore, proinflammatory cytokines like IL‑6 regulate iron metabolism and encourage the formation of Th17 cells, which exacerbates CNS inflammation. Macrophages and microglia, which are implicated in inflammatory responses, collect iron during MS, exacerbating neuroinflammation and demyelination. Disrupted iron homeostasis is a major contributor to MS pathology, with iron deficiency affecting immunological function and changing T‑cell responses, both of which are necessary for disease progression. Lumbar puncture, oligoclonal bands analysis, and magnetic resonance imaging are all used to diagnose MS and confirm disease activity and progression. The blood‑brain barrier is frequently disrupted in MS, allowing the influx of inflammatory cells. The aim of this paper is to demonstrate the cause‑effect relationship between the amount of iron and the health status of patients with MS.

铁在多发性硬化症中的作用——从病理生理学到疾病进展——一篇叙述性文献综述。
多发性硬化症(MS)是一种以脱髓鞘和神经退行性变为特征的慢性自身免疫性疾病,它会导致身体残疾和神经系统的严重改变,包括神经胶质瘤和神经元丢失。这种疾病主要影响中枢神经系统(CNS)的髓鞘部分,如视神经、小脑、脑干和脊髓。T细胞通过诱导脱髓鞘在MS发病中发挥重要作用,其危险因素包括遗传易感性、环境影响和生活方式决定。多发性硬化症的患病率正在上升,特别是在妇女和老年人中。铁调节失调是MS发病机制中的一个关键因素,过量的铁通过铁上吊和免疫反应调节引起神经退行性变。过量的铁通过触发具有炎症特性的巨噬细胞的激活,并促进小胶质细胞向促炎表型极化,从而放大炎症。这会导致氧化应激增加、线粒体功能障碍和活性氧的释放,从而损害神经元。此外,IL - 6等促炎细胞因子调节铁代谢,促进Th17细胞的形成,从而加剧中枢神经系统炎症。巨噬细胞和小胶质细胞参与炎症反应,在MS期间收集铁,加剧神经炎症和脱髓鞘。铁稳态的破坏是MS病理的主要因素,铁缺乏影响免疫功能和改变T细胞反应,这两者都是疾病进展所必需的。腰椎穿刺、寡克隆条带分析和磁共振成像均可用于诊断MS并确认疾病活动和进展。在多发性硬化症中,血脑屏障经常被破坏,使炎症细胞流入。本文的目的是为了证明铁的量与MS患者的健康状况之间的因果关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
2.20
自引率
7.10%
发文量
40
审稿时长
>12 weeks
期刊介绍: Acta Neurobiologiae Experimentalis (ISSN: 0065-1400 (print), eISSN: 1689-0035) covers all aspects of neuroscience, from molecular and cellular neurobiology of the nervous system, through cellular and systems electrophysiology, brain imaging, functional and comparative neuroanatomy, development and evolution of the nervous system, behavior and neuropsychology to brain aging and pathology, including neuroinformatics and modeling.
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