ArticleCNS neuroscience & therapeutics2025
Auricular Transcutaneous Vagus Nerve Stimulation Enhances Post-Stroke Neurological and Cognitive Recovery in Mice by Suppressing Ferroptosis Through α7 Nicotinic Acetylcholine Receptor Activation.
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 8 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effects and mechanisms of transcutaneous auricular vagus nerve stimulation on post-stroke cognitive impairment in animal studies: a systematic review and meta-analysis.Frontiers in neuroscience · 2026Pooled it
- Vagus Nerve Stimulation in Alzheimer's Disease and Mild Cognitive Impairment: Current Evidence and Future Directions.NeuroSci · 2026Review
- Review
- Transcutaneous auricular vagus nerve stimulation: mechanisms, applications, and research progress.Frontiers in neuroscience · 2026Review
- Neuromodulation and rehabilitation of post-stroke cognitive impairment: challenges and prospects.Frontiers in psychiatry · 2026Review
- Clinical advances in transcutaneous auricular vagus nerve stimulation for post-stroke disorders: state of the art and future perspectives.Frontiers in neurology · 2025Review
- Therapeutic potential of transcutaneous auricular vagus nerve stimulation in cognitive impairment: insights from preclinical and clinical studies.Frontiers in neurologyReview
- Efficacy of transcutaneous auricular vagus nerve stimulation in treating patients with post-stroke motor disorders: a prospective study.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
aimsFerroptosis plays a critical role in stroke pathophysiology, yet its dynamics during recovery remain unclear. This study aimed to investigate the evolution of ferroptosis throughout post-stroke recovery and evaluate auricular transcutaneous vagus nerve stimulation (atVNS) as a therapeutic intervention, focusing on the involvement of α7 nicotinic acetylcholine receptor (α7nAChR)-mediated mechanisms.
methodsUsing a middle cerebral artery occlusion (MCAO) mouse model, we examined ferroptosis-related protein expression (GPX4, ACSL4, TfR) and iron levels across acute to chronic recovery phases. The therapeutic effects of atVNS were evaluated through the assessment of ferroptosis markers, neurogenesis, angiogenesis, cognitive function, and neuroinflammation. α7nAChR knockout mice were used to investigate the receptor's role in atVNS-mediated recovery.
resultsWe observed sustained alterations in ferroptosis markers and iron levels throughout post-stroke recovery. atVNS treatment reduced ferroptosis progression by modulating GPX4 and ACSL4 expression, enhanced neurogenesis and angiogenesis, improved cognitive recovery, and reduced neuroinflammation. These beneficial effects were absent in α7nAChR knockout mice, while atVNS increased neuronal α7nAChR expression in wild-type mice.
conclusionsThis study reveals the persistent involvement of ferroptosis in stroke recovery and demonstrates that atVNS provides comprehensive neuroprotection through α7nAChR-dependent mechanisms. These findings establish atVNS as a promising noninvasive therapeutic approach for stroke recovery and highlight α7nAChR signaling as a potential therapeutic target.
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Registered trials
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