Evidence map›Paper›PMID 32350521›Full record

ArticleEuropean heart journal2020

Adipocyte fatty acid-binding protein exacerbates cerebral ischaemia injury by disrupting the blood-brain barrier.

Boya Liao, Leiluo Geng, Fang Zhang, Lingling Shu, Ling Wei, Patrick K K Yeung, Karen S L Lam, Sookja K Chung, Junlei Chang, Paul M Vanhoutte and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in European heart journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
7.7field-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

63 citing papers in PubMed, 108 citations in OpenAlex.

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  9. Monocyte-derived macrophages and their roles in ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
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  17. Piezo1 disrupts blood-brain barrier via CaMKII/Nrf2 in ischemic stroke.Cellular and molecular life sciences : CMLS · 2025
    Article
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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 6 institutions in 4 countries.

Boya LiaoState Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Leiluo GengState Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Fang ZhangDepartment of Radiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, No. 107, Yanjiang Road West, Guangzhou 510120, China.
Lingling ShuState Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Ling WeiDepartment of Neurology, the First Affiliated Hospital of Anhui Medical University, Anhui Province Key Laboratory on Cognition and Neuropsychiatric Disorders, No. 218, Jixi Road, Hefei, Anhui Province 230022, China.
Patrick K K YeungDepartment of Anatomy, School of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Karen S L LamState Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Sookja K ChungDepartment of Anatomy, School of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Junlei ChangCentre for Protein and Cell-based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, No. 1068, Xueyuan Blvd, Xili Nanshan, Shenzhen 518055, China.
Paul M VanhoutteState Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Aimin XuState Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Kai WangDepartment of Neurology, the First Affiliated Hospital of Anhui Medical University, Anhui Province Key Laboratory on Cognition and Neuropsychiatric Disorders, No. 218, Jixi Road, Hefei, Anhui Province 230022, China.
Ruby L C HooState Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
University of Hong Kong · HKAnhui Medical University · CNChinese Academy of Sciences · CNMacau University of Science and Technology · MOSun Yat-sen University · CNUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsAdipocyte fatty acid-binding protein (A-FABP) is an adipokine implicating in various metabolic diseases. Elevated circulating levels of A-FABP correlate positively with poor prognosis in ischaemic stroke (IS) patients. No information is available concerning the role of A-FABP in the pathogenesis of IS. Experiments were designed to determine whether or not A-FABP mediates blood-brain barrier (BBB) disruption, and if so, to explore the molecular mechanisms underlying this deleterious effects. METHODS AND

resultsCirculating A-FABP and its cerebral expression were increased in mice after middle cerebral artery occlusion. Genetic deletion and pharmacological inhibition of A-FABP alleviated cerebral ischaemia injury with reduced infarction volume, cerebral oedema, neurological deficits, and neuronal apoptosis; BBB disruption was attenuated and accompanied by reduced degradation of tight junction proteins and induction of matrix metalloproteinases-9 (MMP-9). In patients with acute IS, elevated circulating A-FABP levels positively correlated with those of MMP-9 and cerebral infarct volume. Mechanistically, ischaemia-induced elevation of A-FABP selectively in peripheral blood monocyte-derived macrophages and cerebral resident microglia promoted MMP-9 transactivation by potentiating JNK/c-Jun signalling, enhancing degradation of tight junction proteins and BBB leakage. The detrimental effects of A-FABP were prevented by pharmacological inhibition of MMP-9.

conclusionA-FABP is a key mediator of cerebral ischaemia injury promoting MMP-9-mediated BBB disruption. Inhibition of A-FABP is a potential strategy to improve IS outcome.

Indexed as

Brain IschemiaStrokeAdipocytesAnimalsBlood-Brain BarrierFatty Acid-Binding ProteinsHumansInfarction, Middle Cerebral ArteryMiceFatty Acid-Binding ProteinsA-FABPBlood–brain barrierIschaemic strokeJNK/c-Jun signallingMMP-9

Identifiers

PMID32350521
PMCPMC7556749
OpenAlexW3021123623

What OpenQuestion holds

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Registered trials

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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.