Evidence map›Paper›PMID 37017889›Full record

ReviewNeurochemical research2023

Ischemia Reperfusion Injury Induced Blood Brain Barrier Dysfunction and the Involved Molecular Mechanism.

Xi Guo, Ru Liu, Meng Jia, Qun Wang, Jianping Wu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
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  17. Tracing Inflammation in Ischemic Stroke: Biomarkers and Clinical Insight.International journal of molecular sciences · 2025
    Review
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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

5 authors at 1 institution in 1 country.

Xi GuoHubei Key Laboratory of Nanomedicine for Neurodegenerative Diseases, School of Chemistry, Chemical Engineering and Life Sciences, Wuhan University of Technology, Wuhan, 430070, China.
Ru LiuHubei Key Laboratory of Nanomedicine for Neurodegenerative Diseases, School of Chemistry, Chemical Engineering and Life Sciences, Wuhan University of Technology, Wuhan, 430070, China.
Meng JiaBeijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Qun WangBeijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Jianping WuHubei Key Laboratory of Nanomedicine for Neurodegenerative Diseases, School of Chemistry, Chemical Engineering and Life Sciences, Wuhan University of Technology, Wuhan, 430070, China. biojpwu@whut.edu.cn.ORCID http://orcid.org/0000-0002-2684-6122
Capital Medical University · CN

Funding

National Natural Science Foundation of China 81870935Natural Science Foundation of Beijing 7214224Scientific Research Found of Wuhan University of Technology 40122070
6 · The paper itself

Abstract

Stroke is characterized by the abrupt failure of blood flow to a specific brain region, resulting in insufficient supply of oxygen and glucose to the ischemic tissues. Timely reperfusion of blood flow can rescue dying tissue but can also lead to secondary damage to both the infarcted tissues and the blood-brain barrier, known as ischemia/reperfusion injury. Both primary and secondary damage result in biphasic opening of the blood-brain barrier, leading to blood-brain barrier dysfunction and vasogenic edema. Importantly, blood-brain barrier dysfunction, inflammation, and microglial activation are critical factors that worsen stroke outcomes. Activated microglia secrete numerous cytokines, chemokines, and inflammatory factors during neuroinflammation, contributing to the second opening of the blood-brain barrier and worsening the outcome of ischemic stroke. TNF-α, IL-1β, IL-6, and other microglia-derived molecules have been shown to be involved in the breakdown of blood-brain barrier. Additionally, other non-microglia-derived molecules such as RNA, HSPs, and transporter proteins also participate in the blood-brain barrier breakdown process after ischemic stroke, either in the primary damage stage directly influencing tight junction proteins and endothelial cells, or in the secondary damage stage participating in the following neuroinflammation. This review summarizes the cellular and molecular components of the blood-brain barrier and concludes the association of microglia-derived and non-microglia-derived molecules with blood-brain barrier dysfunction and its underlying mechanisms.

Indexed as

Brain IschemiaIschemic StrokeReperfusion InjuryStrokeBlood-Brain BarrierEndothelial CellsHumansNeuroinflammatory DiseasesBlood–brain barrierCytokinesIon channelsIschemic strokeMicrogliaTransporters

Identifiers

PMID37017889
OpenAlexW4362601723

What Socratic 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 Socratic graph.