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
{"title":"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。","authors":"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","doi":"10.3390/neurosci6010023","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 1","pages":""},"PeriodicalIF":1.6000,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11944927/pdf/","citationCount":"0","resultStr":"{\"title\":\"The Connection Between Oxidative Stress, Mitochondrial Dysfunction, Iron Metabolism and Microglia in Multiple Sclerosis: A Narrative Review.\",\"authors\":\"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\",\"doi\":\"10.3390/neurosci6010023\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":74294,\"journal\":{\"name\":\"NeuroSci\",\"volume\":\"6 1\",\"pages\":\"\"},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2025-03-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11944927/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"NeuroSci\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3390/neurosci6010023\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"NeuroSci","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/neurosci6010023","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
The Connection Between Oxidative Stress, Mitochondrial Dysfunction, Iron Metabolism and Microglia in Multiple Sclerosis: A Narrative Review.
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.