ArticleTranslational stroke research2018
Hi1a as a Novel Neuroprotective Agent for Ischemic Stroke by Inhibition of Acid-Sensing Ion Channel 1a.
Article in Translational stroke research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- A short peptide exerts neuroprotective effects on cerebral ischemia-reperfusion injury by reducing inflammation via the miR-6328/IKKβ/NF-κB axis.Journal of neuroinflammation · 2023Article
- The Deadly Toxin Arsenal of the Tree-Dwelling Australian Funnel-Web Spiders.International journal of molecular sciences · 2022Article
- Review
- Imaging Acute Stroke: From One-Size-Fit-All to Biomarkers.Frontiers in neurology · 2021Review
- [Acid-sensing ion channels differentially affect ictal-like and non-ictal-like epileptic activities of mouse hippocampal pyramidal neurons in acidotic extracellular pH].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Hederagenin Attenuates Cerebral Ischaemia/Reperfusion Injury by Regulating MLK3 Signalling.Frontiers in pharmacology · 2020Article
- From Animal Poisons and Venoms to Medicines: Achievements, Challenges and Perspectives in Drug Discovery.Frontiers in pharmacology · 2020Review
- Commentary: Potential Therapeutic Consequences of an Acid-Sensing Ion Channel 1a-Blocking Antibody.Frontiers in pharmacology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Strokes are the second-leading cause of death worldwide, and the cellular and molecular mechanisms underlying stroke-induced brain damage are still uncertain. The present therapy for acute ischemic stroke is limited to thrombolysis with the recombinant tissue plasminogen activator (rtPA). However, rtPA has a narrow therapeutic timeframe of 3-4.5 h, and only approximately 5% of stroke patients can benefit from rtPA treatment. Neuroprotective agents, such as N-methyl-D-aspartate receptor antagonists, have shown great promise in preclinical studies. However, due to a limited therapeutic time window and/or intolerable side effects, they have failed in clinical trials. Extending the time window and reducing side effects for neuroprotective drugs against strokes are critical for effective therapy for stroke patients. A recent study published in Proceedings of the National Academy of Sciences by Irène R. Chassagnon et al. (2017) indicates that Hi1a, a disulfide-rich spider venom peptide, is a highly neuroprotective agent in both in vitro and in vivo studies against experimental stroke. Hi1a reveals neuroprotection through inhibition of acid-sensing ion channel 1a. Thus, Hi1a might be a promising neuroprotective agent to protect the brain from ischemic injury in humans.
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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 OpenQuestion graph.