ArticleScientific reports2017
Network-Based Approach to Identify Potential Targets and Drugs that Promote Neuroprotection and Neurorepair in Acute Ischemic Stroke.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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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.
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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
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Citicoline for treating people with acute ischemic stroke.The Cochrane database of systematic reviews · 2020Pooled it
- Deregulated Protein Kinases: Friend and Foe in Ischemic Stroke.Molecular neurobiology · 2021Review
- A network-based machine-learning framework to identify both functional modules and disease genes.Human genetics · 2021Article
- Integrated Modules Analysis to Explore the Molecular Mechanisms of Phlegm-Stasis Cementation Syndrome with Ischemic Heart Disease.Frontiers in physiology · 2018Article
- Prediction of Molecular Mechanisms for LianXia NingXin Formula: A Network Pharmacology Study.Frontiers in physiology · 2018Article
- Reperfusion Activates AP-1 and Heat Shock Response in Donor Kidney Parenchyma after Warm Ischemia.BioMed research international · 2018Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute ischemic stroke (AIS) accounts for more than 80% of the approximately 610,000 new stroke cases worldwide every year. Both ischemia and reperfusion can cause death, damage, and functional changes of affected nerve cells, and these alterations can result in high rates of disability and mortality. Therefore, therapies aimed at increasing neuroprotection and neurorepair would make significant contributions to AIS management. However, with regard to AIS therapies, there is currently a large gap between experimental achievements and practical clinical solutions (EC-GAP-AIS). Here, by integrating curated disease-gene associations and interactome network known to be related to AIS, we investigated the molecular network mechanisms of multi-module structures underlying AIS, which might be relevant to the time frame subtypes of AIS. In addition, the EC-GAP-AIS phenomenon was confirmed and elucidated by the shortest path lengths and the inconsistencies in the molecular functionalities and overlapping pathways between AIS-related genes and drug targets. Furthermore, we identified 23 potential targets (e.g. ADORA3, which is involved in the regulation of cellular reprogramming and the extracellular matrix) and 46 candidate drugs (e.g. felbamate, methylphenobarbital and memantine) that may have value for the treatment of AIS.
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