FGIN-1-27 Mitigates Radiation-induced Mitochondrial Hyperfunction and Cellular Hyperactivation in Cultured Astrocytes

Zhang, Shifeng; Deng, Zhezhi; Qiu, Yuemin; Lu, Gengxin; Wu, Junyu; Huang, Haiwei

doi:10.1016/j.neuroscience.2023.10.017

Cited by 1 publication

(2 citation statements)

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“… 26 Studies have shown that activated microglia release various inflammatory mediators, including IL‐1α, TNF‐α, and complement 1q, which can induce neurotoxic A1‐type astrocytes. 35 , 36 Additionally, reactive astrocytes can secrete IL‐6, TNF‐α, interferon‐gamma (IFN‐γ), and complement factor C3, impacting the phenotype, motility, and phagocytic functions of microglia. 37 Furthermore, radiation activates the MAPK, activator protein 1 (AP‐1), and NF‐κB signaling pathways, resulting in increased expression of inflammatory cytokines IL‐1β, IL‐6, and the inflammatory mediator cyclooxygenase‐2 (COX‐2) in astrocytes, thereby further exacerbating their inflammatory phenotype.…”

Section: Microglial Activation After Radiationmentioning

confidence: 99%

“…Furthermore, the release of pro‐inflammatory cytokines such as PGE2 and IL‐1β by microglia following radiation exposure is identified as a key contributor to phenotypic alterations and reactive gliosis proliferation in astrocytes 26 . Studies have shown that activated microglia release various inflammatory mediators, including IL‐1α, TNF‐α, and complement 1q, which can induce neurotoxic A1‐type astrocytes 35,36 . Additionally, reactive astrocytes can secrete IL‐6, TNF‐α, interferon‐gamma (IFN‐γ), and complement factor C3, impacting the phenotype, motility, and phagocytic functions of microglia 37 .…”

Section: Microglial Activation After Radiationmentioning

confidence: 99%

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Microglia in radiation‐induced brain injury: Cellular and molecular mechanisms and therapeutic potential

Wang,

Tian,

Liu

et al. 2024

CNS Neurosci Ther

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BackgroundRadiation‐induced brain injury is a neurological condition resulting from radiotherapy for malignant tumors, with its underlying pathogenesis still not fully understood. Current hypotheses suggest that immune cells, particularly the excessive activation of microglia in the central nervous system and the migration of peripheral immune cells into the brain, play a critical role in initiating and progressing the injury. This review aimed to summarize the latest advances in the cellular and molecular mechanisms and the therapeutic potential of microglia in radiation‐induced brain injury.MethodsThis article critically examines recent developments in understanding the role of microglia activation in radiation‐induced brain injury. It elucidates associated mechanisms and explores novel research pathways and therapeutic options for managing this condition.ResultsPost‐irradiation, activated microglia release numerous inflammatory factors, exacerbating neuroinflammation and facilitating the onset and progression of radiation‐induced damage. Therefore, controlling microglial activation and suppressing the secretion of related inflammatory factors is crucial for preventing radiation‐induced brain injury. While microglial activation is a primary factor in neuroinflammation, the precise mechanisms by which radiation prompts this activation remain elusive. Multiple signaling pathways likely contribute to microglial activation and the progression of radiation‐induced brain injury.ConclusionsThe intricate microenvironment and molecular mechanisms associated with radiation‐induced brain injury underscore the crucial roles of immune cells in its onset and progression. By investigating the interplay among microglia, neurons, astrocytes, and peripheral immune cells, potential strategies emerge to mitigate microglial activation, reduce the release of inflammatory agents, and impede the entry of peripheral immune cells into the brain.

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