ArticleCNS neuroscience & therapeutics2025
Gastrodin Attenuates Cerebral Ischemia-Reperfusion Injury by Enhancing Mitochondrial Fusion and Activating the AMPK-OPA1 Signaling Pathway.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- TMC6 Protects Against Ischemic Neuronal Injury by Activating Rap1/Rac1 Signaling to Restore Mitochondrial Dynamics and Mitophagy.Molecular neurobiology · 2026Article
- Multi-omics analysis of untargeted metabolomics and gut microbiota study on the mechanism of Astragalus-Safflower to coordinate the regulation of energy metabolism pathways and gut microbiota remodeling to improve ischemic stroke.Metabolic brain disease · 2026Article
- Advances in the Core Role and Mechanisms of Mitochondrial Dysfunction in Alzheimer's Disease.Brain and behavior · 2026Review
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- Gastrodin Attenuates Cerebral Ischemia-Reperfusion Injury by Enhancing Mitochondrial Fusion and Activating the AMPK-OPA1 Signaling Pathway.CNS neuroscience & therapeutics · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundCerebral ischemia-reperfusion (I/R) injury is a critical pathological process in stroke, characterized by disrupted energy metabolism, inflammatory responses, and mitochondrial dysfunction. Targeting mitochondrial dynamics presents promising strategies for alleviating brain injury. This study investigates the role and mechanism of Gastrodin (Gas) in regulating mitochondrial dynamics and mitigating cerebral I/R injury via activation of the AMPK-OPA1 signaling pathway.
methodsAn in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model and an in vivo middle cerebral artery occlusion/reperfusion (MCAO/R) model were used to assess the effects of Gas on inflammation, mitochondrial function, and energy metabolism. Immunofluorescence, western blotting (WB), reverse-transcription PCR (RT-PCR), JC-1 staining, and molecular docking techniques were employed for analysis.
resultsGas activated the AMPK-OPA1 signaling pathway, promoting mitochondrial fusion, restoring membrane potential, enhancing ATP production, and rebalancing NAD
conclusionGas alleviates cerebral I/R injury by regulating mitochondrial dynamics via the AMPK-OPA1 signaling pathway. These findings provide a theoretical basis for the therapeutic application of Gas in stroke and offer new insights into mitochondrial-targeted treatment strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.