Evidence map›Paper›PMID 34501242›Full record

ReviewJournal of clinical medicine2021

Caveolae-Mediated Endothelial Transcytosis across the Blood-Brain Barrier in Acute Ischemic Stroke.

Min Zhou, Samuel X Shi, Ning Liu, Yinghua Jiang, Mardeen S Karim, Samuel J Vodovoz, Xiaoying Wang, Boli Zhang, Aaron S Dumont

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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. Article
  2. Temporal enhancement patterns on 3D-FLAIR MRI in labyrinthine infarction.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  3. Article
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  13. Article
  14. Article
  15. Article
  16. Review
  17. Physiological functions of caveolae in endothelium.Current opinion in physiology · 2023
    Article
  18. Review
  19. Review
  20. Review
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

9 authors.

Min ZhouDepartment of Traditional Chinese Medicine, Tianjin Medical University General Hospital, Tianjin 300052, China.
Samuel X ShiClinical Neuroscience Research Center, Department of Neurosurgery, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Ning LiuClinical Neuroscience Research Center, Department of Neurosurgery, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Yinghua JiangClinical Neuroscience Research Center, Department of Neurosurgery, Tulane University School of Medicine, New Orleans, LA 70112, USA.ORCID 0000-0002-7344-7028
Mardeen S KarimClinical Neuroscience Research Center, Department of Neurosurgery, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Samuel J VodovozClinical Neuroscience Research Center, Department of Neurosurgery, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Xiaoying WangClinical Neuroscience Research Center, Department of Neurosurgery, Tulane University School of Medicine, New Orleans, LA 70112, USA.ORCID 0000-0003-3636-7931
Boli ZhangTianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China.
Aaron S DumontClinical Neuroscience Research Center, Department of Neurosurgery, Tulane University School of Medicine, New Orleans, LA 70112, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blood-brain barrier (BBB) disruption following ischemic stroke (IS) contributes to hemorrhagic transformation, brain edema, increased neural dysfunction, secondary injury, and mortality. Brain endothelial cells form a para and transcellular barrier to most blood-borne solutes via tight junctions (TJs) and rare transcytotic vesicles. The prevailing view attributes the destruction of TJs to the resulting BBB damage following IS. Recent studies define a stepwise impairment of the transcellular barrier followed by the paracellular barrier which accounts for the BBB leakage in IS. The increased endothelial transcytosis that has been proven to be caveolae-mediated, precedes and is independent of TJs disintegration. Thus, our understanding of post stroke BBB deficits needs to be revised. These recent findings could provide a conceptual basis for the development of alternative treatment strategies. Presently, our concept of how BBB endothelial transcytosis develops is incomplete, and treatment options remain limited. This review summarizes the cellular structure and biological classification of endothelial transcytosis at the BBB and reviews related molecular mechanisms. Meanwhile, relevant transcytosis-targeted therapeutic strategies for IS and research entry points are prospected.

Indexed as

blood-brain barriercaveolaeischemic stroketranscytosis

Identifiers

PMID34501242
PMCPMC8432094

What OpenQuestion holds

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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.