Evidence map›Paper›PMID 30379577›Full record

ReviewAmerican journal of physiology. Cell physiology2019

Neuroinflammatory mechanisms of blood-brain barrier damage in ischemic stroke.

Changjun Yang, Kimberly E Hawkins, Sylvain Doré, Eduardo Candelario-Jalil

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 515 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
515citing papers in PubMed, 3 pooled it
20.6field-weighted citation impact, top 1% 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

515 citing papers in PubMed, 3 syntheses or guidelines pooled it, 821 citations in OpenAlex.

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455 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Changjun YangDepartment of Neuroscience, McKnight Brain Institute, University of Florida , Gainesville, Florida.
Kimberly E HawkinsDepartment of Neuroscience, McKnight Brain Institute, University of Florida , Gainesville, Florida.
Sylvain DoréDepartment of Neuroscience, McKnight Brain Institute, University of Florida , Gainesville, Florida.
Eduardo Candelario-JalilDepartment of Neuroscience, McKnight Brain Institute, University of Florida , Gainesville, Florida.ORCID 0000-0003-3631-1989
University of Florida · US

Funding

Better Understanding of the Neuroprotective Mechanisms of Korean Ginseng in StrokR01AT007429 · NCCIH · UNIVERSITY OF FLORIDA · PI DORE, SYLVAIN · 2012 to 2016
$2.2M
Cyclooxygenase-2 Regulation of Blood-Brain Barrier Opening in Ischemic StrokeR01NS065849 · NINDS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI CANDELARIO-JALIL, EDUARDO JESUS · 2011 to 2015
$1.5M
Neurovascular Protection by Adropin in Ischemic StrokeR01NS103094 · NINDS · UNIVERSITY OF FLORIDA · PI CANDELARIO-JALIL, EDUARDO JESUS · 2018 to 2021
$1.5M
Neurovascular Protection by Adropin in Ischemic StrokeR56NS103094 · NINDS · UNIVERSITY OF FLORIDA · PI CANDELARIO-JALIL, EDUARDO JESUS · 2017 to 2017
$427k
Regulation and Implication of Hemoglobin Clearance in Subarachnoid Hemorrhagic PatientsR21NS095166 · NINDS · UNIVERSITY OF FLORIDA · PI DORE, SYLVAIN · 2016 to 2017
$426k
NCCIH NIH HHS R01 AT007429NINDS NIH HHS R01 NS065849NINDS NIH HHS R01 NS103094NINDS NIH HHS R21 NS095166NINDS NIH HHS R56 NS103094
6 · The paper itself

Abstract

As part of the neurovascular unit, the blood-brain barrier (BBB) is a unique, dynamic regulatory boundary that limits and regulates the exchange of molecules, ions, and cells between the blood and the central nervous system. Disruption of the BBB plays an important role in the development of neurological dysfunction in ischemic stroke. Blood-borne substances and cells have restricted access to the brain due to the presence of tight junctions between the endothelial cells of the BBB. Following stroke, there is loss of BBB tight junction integrity, leading to increased paracellular permeability, which results in vasogenic edema, hemorrhagic transformation, and increased mortality. Thus, understanding principal mediators and molecular mechanisms involved in BBB disruption is critical for the development of novel therapeutics to treat ischemic stroke. This review discusses the current knowledge of how neuroinflammation contributes to BBB damage in ischemic stroke. Specifically, we provide an updated overview of the role of cytokines, chemokines, oxidative and nitrosative stress, adhesion molecules, matrix metalloproteinases, and vascular endothelial growth factor as well as the role of different cell types in the regulation of BBB permeability in ischemic stroke.

Indexed as

AnimalsBiological TransportBlood-Brain BarrierBrain IschemiaEndothelial CellsHumansInflammation MediatorsOxidative StressPermeabilityStrokeTight JunctionsInflammation Mediatorsblood-brain barrierchemokinescytokinesfocal cerebral ischemiamatrix metalloproteinasesmiddle cerebral artery occlusionneurovascular injuryoxidative stresstight junction proteins

Identifiers

PMID30379577
PMCPMC6397344
OpenAlexW2899197889

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.