Evidence map›Paper›PMID 32855530›Full record

ArticleActa pharmacologica Sinica2020

Drug development in targeting ion channels for brain edema.

Zheng-Wei Luo, Andrea Ovcjak, Raymond Wong, Bao-Xue Yang, Zhong-Ping Feng, Hong-Shuo Sun

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  13. Aquaporins: Gatekeepers of Fluid Dynamics in Traumatic Brain Injury.International journal of molecular sciences · 2024
    Review
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  15. Inhibition of EphA4 reduces vasogenic edema after experimental stroke in mice by protecting the blood-brain barrier integrity.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Zheng-Wei LuoDepartment of Surgery, Faculty of Medicine, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Andrea OvcjakDepartment of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Raymond WongDepartment of Surgery, Faculty of Medicine, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Bao-Xue YangDepartment of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Zhong-Ping FengDepartment of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, M5S 1A8, Canada. zp.feng@utoronto.ca.
Hong-Shuo SunDepartment of Surgery, Faculty of Medicine, University of Toronto, Toronto, ON, M5S 1A8, Canada. hss.sun@utoronto.ca.
University of Toronto · CAPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral edema is a pathological hallmark of various central nervous system (CNS) insults, including traumatic brain injury (TBI) and excitotoxic injury such as stroke. Due to the rigidity of the skull, edema-induced increase of intracranial fluid significantly complicates severe CNS injuries by raising intracranial pressure and compromising perfusion. Mortality due to cerebral edema is high. With mortality rates up to 80% in severe cases of stroke, it is the leading cause of death within the first week. Similarly, cerebral edema is devastating for patients of TBI, accounting for up to 50% mortality. Currently, the available treatments for cerebral edema include hypothermia, osmotherapy, and surgery. However, these treatments only address the symptoms and often elicit adverse side effects, potentially in part due to non-specificity. There is an urgent need to identify effective pharmacological treatments for cerebral edema. Currently, ion channels represent the third-largest target class for drug development, but their roles in cerebral edema remain ill-defined. The present review aims to provide an overview of the proposed roles of ion channels and transporters (including aquaporins, SUR1-TRPM4, chloride channels, glucose transporters, and proton-sensitive channels) in mediating cerebral edema in acute ischemic stroke and TBI. We also focus on the pharmacological inhibitors for each target and potential therapeutic strategies that may be further pursued for the treatment of cerebral edema.

Indexed as

AnimalsBrain EdemaBrain Injuries, TraumaticDrug DevelopmentHumansInfarction, Middle Cerebral ArteryIon ChannelsNeuroprotective AgentsStrokeIon ChannelsNeuroprotective Agentscerebral edemaion channelsischemic stroketransporterstraumatic brain injury

Identifiers

PMID32855530
PMCPMC7609292
OpenAlexW3080575181

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.