ArticleActa pharmaceutica Sinica. B2023
Glutamate-releasing BEST1 channel is a new target for neuroprotection against ischemic stroke with wide time window.
Article in Acta pharmaceutica Sinica. B, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Engineering Extracellular Vesicles for Anti-Aging Therapy: Mechanisms, Applications, and Perspectives.Aging cell · 2026Review
- A modified tail suspension test for the assessment of behavioral despair in mice after stroke.Acta pharmacologica Sinica · 2026Article
- Ellagic acid can improve stroke by regulating gut microbiota.Metabolic brain disease · 2026Review
- Astrocytic BEST1 can serve as a target for functional recovery after ischemic stroke.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The pentameric chloride channel BEST1 is activated by extracellular GABA.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A quantitative analysis of bestrophin 1 cellular localization in mouse cerebral cortex.Acta physiologica (Oxford, England) · 2025Article
- The role of the cerebellum in anoxic-irschemic brain damage and neurological clinical trials.Brain & spine · 2024Article
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Authors and funding
13 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Many efforts have been made to understand excitotoxicity and develop neuroprotectants for the therapy of ischemic stroke. The narrow treatment time window is still to be solved. Given that the ischemic core expanded over days, treatment with an extended time window is anticipated. Bestrophin 1 (BEST1) belongs to a bestrophin family of calcium-activated chloride channels. We revealed an increase in neuronal BEST1 expression and function within the peri-infarct from 8 to 48 h after ischemic stroke in mice. Interfering the protein expression or inhibiting the channel function of BEST1 by genetic manipulation displayed neuroprotective effects and improved motor functional deficits. Using electrophysiological recordings, we demonstrated that extrasynaptic glutamate release through BEST1 channel resulted in delayed excitotoxicity. Finally, we confirmed the therapeutic efficacy of pharmacological inhibition of BEST1 during 6-72 h post-ischemia in rodents. This delayed treatment prevented the expansion of infarct volume and the exacerbation of neurological functions. Our study identifies the glutamate-releasing BEST1 channel as a potential therapeutic target against ischemic stroke with a wide time window.
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