The Connection Between Oxidative Stress, Mitochondrial Dysfunction, Iron Metabolism and Microglia in Multiple Sclerosis: A Narrative Review.

IF 1.6 Q3 CLINICAL NEUROLOGY
NeuroSci Pub Date : 2025-03-04 DOI:10.3390/neurosci6010023
Simonida Delic, Svetlana Miletic Drakulic, Milos Stepovic, Jovana Milosavljevic, Marija Kovacevic Dimitrijevic, Kristijan Jovanovic, Ivona Marinkovic, Melanija Tepavcevic, Nikoleta Janicijevic, Aleksandra Mitrovic, Danica Igrutinovic, Maja Vulovic
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引用次数: 0

Abstract

In recent years, in the pathogenesis of multiple sclerosis, emphasis has been placed on mitochondrial processes that influence the onset of the disease. Oxidative stress would be one of the consequences of mitochondrial dysfunction, and its impact on brain tissue is well described. Microglia, as a brain macrophage, have an important function in removing unwanted metabolites, as well as iron, which is an amplifier of oxidative stress. There are novelties in terms of the connection between these processes, which have redirected research more towards the process of neurodegeneration itself, so that the emphasis is no longer on neuroinflammation, which would initiate the pathological process itself and still exist in the vicinity of lesions with reduced intensity. The aim of this review is to summarize the current knowledge from the literature regarding oxidative stress, mitochondrial dysfunction and iron metabolism and how microglia are involved in these processes in multiple sclerosis.

氧化应激、线粒体功能障碍、铁代谢和多发性硬化症小胶质细胞之间的联系:叙述性综述。
近年来,在多发性硬化症的发病机制中,重点放在影响疾病发病的线粒体过程上。氧化应激可能是线粒体功能障碍的后果之一,它对脑组织的影响已经得到了很好的描述。小胶质细胞作为一种脑巨噬细胞,在清除不需要的代谢物和铁元素方面具有重要作用,铁元素是氧化应激的放大器。这些过程之间的联系有一些新颖之处,这使研究更多地转向神经退行性变本身的过程,因此重点不再放在神经炎症上,神经炎症会启动病理过程本身,并且仍然存在于病变附近,强度降低。这篇综述的目的是总结目前文献中关于氧化应激、线粒体功能障碍和铁代谢的知识,以及小胶质细胞如何参与多发性硬化症的这些过程。
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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