ArticleBrain and behavior2025
Unraveling the Role of α2δ-1 in Cerebral Hemorrhage: Calcium Overload, Endoplasmic Reticulum Stress, and Microglial Apoptosis.
Article in Brain and behavior, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Calcium overload induces reactive oxygen species to enhance glioblastoma radiosensitivity.Medical gas research · 2026Article
- Neuroprotection After Intracerebral Hemorrhage: Apoptosis, Neurogenesis, and Prospects of Stem Cell Therapy.Stem cells international · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
objectiveCerebral hemorrhage is a severe condition associated with high morbidity and mortality. Understanding the underlying pathogenesis is crucial for developing effective therapeutic strategies. This study aimed to investigate the role of the dysregulated α2δ-1 protein in cerebral hemorrhage. MATERIALS AND
methodsWe observed a significant upregulation of α2δ-1 in cerebral hemorrhage tissue. Knockdown of α2δ-1 resulted in decreased intracellular calcium concentration and reduced phosphorylation of PLCr and IP3R in the presence of calcium. Additionally, α2δ-1-mediated calcium overload induced ERS in BV2 microglia, accompanied with increased phosphorylation of PERK and decreased ERS-related protein levels.
resultsα2δ-1 knockdown significantly inhibited BV2 microglia apoptosis and downregulated apoptosis-related proteins in the presence of calcium. Our study indicates the involvement of α2δ-1 in calcium-mediated signaling, endoplasmic reticulum stress, and BV2 microglia apoptosis.
conclusionsThe findings provide a basis for considering α2δ-1 as a potential therapeutic target in cerebral hemorrhage and secondary brain injury conditions associated with calcium dysregulation.
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