Evidence map›Paper›PMID 38439960›Full record

ArticleiScience2024

Trifluoperazine regulates blood-brain barrier permeability via the MLCK/p-MLC pathway to promote ischemic stroke recovery.

Wentao Zhang, Sisi Chen, Bin Ma, Yingmei Ding, Xiaofen Liu, Caijun He, Biao Wang, Mei Yuan

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

Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Wentao ZhangThe Second Affiliated Hospital, Department of Neurology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Sisi ChenThe Second Affiliated Hospital, Department of Neurology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Bin MaThe Second Affiliated Hospital, Department of Neurology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Yingmei DingThe Second Affiliated Hospital, Department of Neurology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Xiaofen LiuThe Second Affiliated Hospital, Department of Neurology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Caijun HeThe Second Affiliated Hospital, Department of Neurology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Biao WangThe Second Affiliated Hospital, Department of Neurology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Mei YuanThe Second Affiliated Hospital, Department of Neurology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blood-brain barrier (BBB) disruption following ischemic stroke (IS) can induce significant aftereffects. Elevated calmodulin (CaM) expression following stroke causes calcium overload-a key contributor to BBB collapse. Trifluoperazine (TFP), a CaM inhibitor, reduces CaM overexpression following IS. However, it remains unclear whether TFP participates in BBB repair after IS. We administered TFP to mice subjected to middle cerebral artery occlusion (MCAO) and bEnd.3 cells subjected to oxygen-glucose deprivation (OGD). TFP treatment in MCAO mice reduced cerebral CaM expression and infarct size and decreased BBB permeability. OGD-treated bEnd.3 cells showed significantly increased CaM protein levels and reduced tight junction (TJ) protein levels; these changes were reversed by TFP treatment. Our results found that TFP administration in mice inhibited actin contraction following cerebral ischemia-reperfusion by suppressing the MLCK/p-MLC pathway, thereby attenuating cell retraction, improving TJ protein integrity, and reducing BBB permeability. Consequently, this treatment may promote neurological function recovery after IS.

Indexed as

Molecular biologyPhysiology

Identifiers

PMID38439960
PMCPMC10910233
OpenAlexW4391788306

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.