Evidence map›Paper›PMID 29888120›Full record

ArticleBiochemistry & pharmacology : open access2016

Ischemia-reperfusion Injury in the Brain: Mechanisms and Potential Therapeutic Strategies.

Lin L, Wang X, Yu Z

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochemistry & pharmacology : open access, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 7% 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

139 citing papers in PubMed, 2 syntheses or guidelines pooled it, 275 citations in OpenAlex.

  1. Pooled it
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  15. Drug Design for Cerebral Ischemia: A Molecular Perspective Review.CNS & neurological disorders drug targets · 2026
    Review
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79 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

3 authors at 2 institutions in 1 country.

Lin LInstitute of Molecular Pharmacology, Wenzhou Medical University, Wenzhou 325035, PR China.
Wang XDepartments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Yu ZDepartments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Harvard University · USMassachusetts General Hospital · US

Funding

Neuroprotective Mechanisms of Neuroglobin in StrokeR01NS049476 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI WANG, XIAOYING · 2006 to 2010
$1.7M
NINDS NIH HHS R01 NS049476
6 · The paper itself

Abstract

Ischemia-reperfusion injury is a common feature of ischemic stroke, which occurs when blood supply is restored after a period of ischemia. Reperfusion can be achieved either by thrombolysis using thrombolytic reagents such as tissue plasminogen activator (tPA), or through mechanical removal of thrombi. Spontaneous reperfusion also occurs after ischemic stroke. However, despite the beneficial effect of restored oxygen supply by reperfusion, it also causes deleterious effect compared with permanent ischemia. With the recent advancement in endovascular therapy including thrombectomy and thrombus disruption, reperfusion-injury has become an increasingly critical challenge in stroke treatment. It is therefore of extreme importance to understand the mechanisms of ischemia-reperfusion injury in the brain in order to develop effective therapeutics. Accumulating experimental evidence have suggested that the mechanisms of ischemia-reperfusion injury include oxidative stress, leukocyte infiltration, platelet adhesion and aggregation, complement activation, mitochondrial mediated mechanisms, and blood-brain-barrier (BBB) disruption, which altogether ultimately lead to edema or hemorrhagic transformation (HT) in the brain. Potential therapeutic strategies against ischemia-reperfusion injury may be developed targeting these mechanisms. In this review, we briefly discuss the pathophysiology and cellular and molecular mechanisms of cerebral ischemia-reperfusion injury, and potential therapeutic strategies.

Indexed as

Blood-brain-barrierComplementIschemiaLeukocyteMitochondriaOxidative stressPlatelet aggregationPost-conditioningReperfusionStroke

Identifiers

PMID29888120
PMCPMC5991620
OpenAlexW2518892410

What OpenQuestion holds

Textmetadata
LicenceTDM
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.