Evidence map›Paper›PMID 33939120›Full record

ArticleNeuroscience bulletin2021

Acrolein Induces Systemic Coagulopathy via Autophagy-dependent Secretion of von Willebrand Factor in Mice after Traumatic Brain Injury.

Wenxing Cui, Xun Wu, Dayun Feng, Jianing Luo, Yingwu Shi, Wei Guo, Haixiao Liu, Qiang Wang, Liang Wang, Shunnan Ge and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Neuroscience bulletin, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

12 citing papers in PubMed, 13 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

11 authors at 1 institution in 1 country.

Wenxing Cui *Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Xun Wu *Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Dayun Feng *Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Jianing LuoDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Yingwu ShiDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Wei GuoDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Haixiao LiuDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Qiang WangDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Liang WangDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Shunnan GeDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China. gesn8561@fmmu.edu.cn.
Yan QuDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China. yanqu0123@fmmu.edu.cn.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI)-induced coagulopathy has increasingly been recognized as a significant risk factor for poor outcomes, but the pathogenesis remains poorly understood. In this study, we aimed to investigate the causal role of acrolein, a typical lipid peroxidation product, in TBI-induced coagulopathy, and further explore the underlying molecular mechanisms. We found that the level of plasma acrolein in TBI patients suffering from coagulopathy was higher than that in those without coagulopathy. Using a controlled cortical impact mouse model, we demonstrated that the acrolein scavenger phenelzine prevented TBI-induced coagulopathy and recombinant ADAMTS-13 prevented acrolein-induced coagulopathy by cleaving von Willebrand factor (VWF). Our results showed that acrolein may contribute to an early hypercoagulable state after TBI by regulating VWF secretion. mRNA sequencing (mRNA-seq) and transcriptome analysis indicated that acrolein over-activated autophagy, and subsequent experiments revealed that acrolein activated autophagy partly by regulating the Akt/mTOR pathway. In addition, we demonstrated that acrolein was produced in the perilesional cortex, affected endothelial cell integrity, and disrupted the blood-brain barrier. In conclusion, in this study we uncovered a novel pro-coagulant effect of acrolein that may contribute to TBI-induced coagulopathy and vascular leakage, providing an alternative therapeutic target.

Indexed as

Blood Coagulation DisordersBrain Injuries, TraumaticAcroleinAnimalsAutophagyHumansMicevon Willebrand FactorAcroleinvon Willebrand FactorAcroleinAutophagyCoagulopathyTraumatic brain injuryVon Willebrand factor

Identifiers

PMID33939120
PMCPMC8353051
OpenAlexW3189709223

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.