ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025
Astrocytic BEST1 can serve as a target for functional recovery after ischemic stroke.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- TRIM21 Exacerbates Ischemic Brain Injury by Promoting Astrocyte-Mediated Neuroinflammation via K63-Linked Ubiquitination of MDA5.Research (Washington, D.C.) · 2026Article
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12 authors.
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Abstract
Solid evidence from animal experiments supported the concept of peri-infarct tonic inhibition. Related drug targets have the potential to be translated for clinical stroke treatment. Recently, we reported the contribution of neuronal bestrophin-1 (BEST1)-mediated glutamate release to acute ischemic damage exacerbation in rodents. Now, we found a switch of abnormal BEST1 expression and function from neurons to astrocytes in the peri-infarct cortex following astrocytic activation. Excessive GABA was released through astrocytic BEST1 channel during the subacute phase of stroke, leading to sustained tonic inhibition. Astrocyte-specific knockdown of BEST1 promoted motor functional recovery, depending on reduced tonic inhibition. Moreover, we prepared self-assembled nanoparticles encapsulating siBest1 (SNP-siBest1), which displayed high brain accumulation and long circulation and knocked down astrocytic BEST1 effectively and safely. Systemic treatment with SNP-siBest1 after ischemic stroke showed a therapeutic effect in mice. Therefore, BEST1 is a potential target for stroke therapy from acute to subacute phase, and selective BEST1 blockers beyond nanoparticles are worth developing.
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