Neuroinflammation and iron metabolism after intracerebral hemorrhage: a glial cell perspective
Intracerebral hemorrhage (ICH) is the most common subtype of hemorrhagic stroke causing significant morbidity and mortality. Previously clinical treatments for ICH have largely been based on a single pathophysiological perspective, and there remains a lack of curative interventions. Following the ru...
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Frontiers Media S.A.
2025-01-01
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| Series: | Frontiers in Neurology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fneur.2024.1510039/full |
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| author | Jia-Jun Ju Li-Hua Hang Li-Hua Hang |
| author_facet | Jia-Jun Ju Li-Hua Hang Li-Hua Hang |
| author_sort | Jia-Jun Ju |
| collection | DOAJ |
| description | Intracerebral hemorrhage (ICH) is the most common subtype of hemorrhagic stroke causing significant morbidity and mortality. Previously clinical treatments for ICH have largely been based on a single pathophysiological perspective, and there remains a lack of curative interventions. Following the rupture of cerebral blood vessels, blood metabolites activate resident immune cells such as microglia and astrocytes, and infiltrate peripheral immune cells, leading to the release of a series of inflammatory mediators. Degradation of hemoglobin produces large amounts of iron ions, leading to an imbalance of iron homeostasis and the production of large quantities of harmful hydroxyl radicals. Neuroinflammation and dysregulation of brain iron metabolism are both important pathophysiological changes in ICH, and both can exacerbate secondary brain injury. There is an inseparable relationship between brain iron metabolism disorder and activated glial cells after ICH. Glial cells participate in brain iron metabolism through various mechanisms; meanwhile, iron accumulation exacerbates neuroinflammation by activating inflammatory signaling pathways modulating the functions of inflammatory cells, and so on. This review aims to explore neuroinflammation from the perspective of iron metabolism, linking the complex pathophysiological changes, delving into the exploration of treatment approaches for ICH, and offering insights that could enhance clinical management strategies. |
| format | Article |
| id | doaj-art-bcc849b1deeb4109b7e477262cda514d |
| institution | DOAJ |
| issn | 1664-2295 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Frontiers Media S.A. |
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| series | Frontiers in Neurology |
| spelling | doaj-art-bcc849b1deeb4109b7e477262cda514d2025-08-20T03:01:39ZengFrontiers Media S.A.Frontiers in Neurology1664-22952025-01-011510.3389/fneur.2024.15100391510039Neuroinflammation and iron metabolism after intracerebral hemorrhage: a glial cell perspectiveJia-Jun Ju0Li-Hua Hang1Li-Hua Hang2Gusu School, Nanjing Medical University, The First People’s Hospital of Kunshan, Kunshan, ChinaGusu School, Nanjing Medical University, The First People’s Hospital of Kunshan, Kunshan, ChinaKunshan Cancer Pain Prevention and Treatment Key Laboratory, Kunshan, ChinaIntracerebral hemorrhage (ICH) is the most common subtype of hemorrhagic stroke causing significant morbidity and mortality. Previously clinical treatments for ICH have largely been based on a single pathophysiological perspective, and there remains a lack of curative interventions. Following the rupture of cerebral blood vessels, blood metabolites activate resident immune cells such as microglia and astrocytes, and infiltrate peripheral immune cells, leading to the release of a series of inflammatory mediators. Degradation of hemoglobin produces large amounts of iron ions, leading to an imbalance of iron homeostasis and the production of large quantities of harmful hydroxyl radicals. Neuroinflammation and dysregulation of brain iron metabolism are both important pathophysiological changes in ICH, and both can exacerbate secondary brain injury. There is an inseparable relationship between brain iron metabolism disorder and activated glial cells after ICH. Glial cells participate in brain iron metabolism through various mechanisms; meanwhile, iron accumulation exacerbates neuroinflammation by activating inflammatory signaling pathways modulating the functions of inflammatory cells, and so on. This review aims to explore neuroinflammation from the perspective of iron metabolism, linking the complex pathophysiological changes, delving into the exploration of treatment approaches for ICH, and offering insights that could enhance clinical management strategies.https://www.frontiersin.org/articles/10.3389/fneur.2024.1510039/fullintracerebral hemorrhageneuroinflammationiron metabolismmicrogliaastrocytesoligodendrocytes |
| spellingShingle | Jia-Jun Ju Li-Hua Hang Li-Hua Hang Neuroinflammation and iron metabolism after intracerebral hemorrhage: a glial cell perspective Frontiers in Neurology intracerebral hemorrhage neuroinflammation iron metabolism microglia astrocytes oligodendrocytes |
| title | Neuroinflammation and iron metabolism after intracerebral hemorrhage: a glial cell perspective |
| title_full | Neuroinflammation and iron metabolism after intracerebral hemorrhage: a glial cell perspective |
| title_fullStr | Neuroinflammation and iron metabolism after intracerebral hemorrhage: a glial cell perspective |
| title_full_unstemmed | Neuroinflammation and iron metabolism after intracerebral hemorrhage: a glial cell perspective |
| title_short | Neuroinflammation and iron metabolism after intracerebral hemorrhage: a glial cell perspective |
| title_sort | neuroinflammation and iron metabolism after intracerebral hemorrhage a glial cell perspective |
| topic | intracerebral hemorrhage neuroinflammation iron metabolism microglia astrocytes oligodendrocytes |
| url | https://www.frontiersin.org/articles/10.3389/fneur.2024.1510039/full |
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