ArticleJournal of the American Heart Association2025
Downregulation of the HCN1 Channel Alleviates Anxiety- and Depression-Like Behaviors in Mice With Cerebral Ischemia-Reperfusion Injury by Suppressing the NLRP3 Inflammasome.
Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Natural antidepressants in neuroimmunomodulation: molecular mechanisms, action targets, and therapeutic potential.Frontiers in immunology · 2025Pooled it
- Synaptic Plasticity-Intrinsic Excitability and Antidepressant Discovery.Biomedicines · 2026Review
- Shared Mechanisms and Integrated Management of Post-Stroke Pain and Depression: A Comprehensive Review.Pain and therapy · 2026Review
- Central Neurobiological Mechanisms of Acupuncture in Post-Stroke Depression: Multi-Target and Network-Based Regulation.Neuropsychiatric disease and treatment · 2026Review
- Correlation between anxiety-depression disorders and brain structural connectivity abnormalities after subarachnoid hemorrhage.World journal of psychiatry · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPost-stroke depression (PSD) is a prevalent neuropsychiatric complication of stroke. However, the mechanisms underlying PSD are still unclear. Here, we aimed to investigate the role of HCN1 (hyperpolarization-activated cyclic nucleotide-gated cation channel 1) in the pathogenesis of PSD and its underlying mechanisms.
methodsThe PSD mice model was established by middle cerebral artery occlusion in vivo. Four weeks after middle cerebral artery occlusion, anxiety- and depression-like behaviors of mice were evaluated by various behavioral tests. HCN channels were downregulated by pharmacological inhibitor or neuron-specific adeno-associated virus. The oxygen-glucose deprivation/reoxygenation model in SY5Y cells was used to study the pathogenesis of PSD in vitro.
resultsMice exhibited anxiety- and depression-like behavior 4 weeks after middle cerebral artery occlusion, along with a significant increase in HCN1 protein expression in the ischemic hippocampus. Furthermore, the I
conclusionsDownregulation of HCN1 channels has a beneficial effect on PSD by suppressing the NLRP3 inflammasome pathway, thus offering promise as a strategy for preventing and treating PSD.
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Registered trials
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