Evidence map›Paper›PMID 32733436›Full record

ArticleFrontiers in immunology2020

TMEM16F Aggravates Neuronal Loss by Mediating Microglial Phagocytosis of Neurons in a Rat Experimental Cerebral Ischemia and Reperfusion Model.

Yijie Zhang, Haiying Li, Xiang Li, Jie Wu, Tao Xue, Jiang Wu, Haitao Shen, Xiang Li, Meifen Shen, Gang Chen

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

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  11. Impacts of Oxylipins on ischemic stroke: from pathophysiology to clinical phenotypes.Metabolomics : Official journal of the Metabolomic Society · 2025
    Review
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  19. TMEM16F exacerbates tau pathology and mediates phosphatidylserine exposure in phospho-tau-burdened neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  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

10 authors at 2 institutions in 1 country.

Yijie ZhangBrain and Nerve Research Laboratory, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Haiying LiBrain and Nerve Research Laboratory, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Xiang LiBrain and Nerve Research Laboratory, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Jie WuBrain and Nerve Research Laboratory, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Tao XueBrain and Nerve Research Laboratory, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Jiang WuBrain and Nerve Research Laboratory, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Haitao ShenBrain and Nerve Research Laboratory, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Xiang LiBrain and Nerve Research Laboratory, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Meifen ShenBrain and Nerve Research Laboratory, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Gang ChenBrain and Nerve Research Laboratory, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
First Affiliated Hospital of Soochow University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral ischemia is a severe, acute condition, normally caused by cerebrovascular disease, and results in high rates of disability, and death. Phagoptosis is a newly recognized form of cell death caused by phagocytosis of viable cells, and has been reported to contribute to neuronal loss in brain tissue after ischemic stroke. Previous data indicated that exposure of phosphatidylserine to viable neurons could induce microglial phagocytosis of such neurons. Phosphatidylserine can be reversibly exposed to viable cells as a result of a calcium-activated phospholipid scramblase named TMEM16F. TMEM16F-mediated phospholipid scrambling on platelet membranes is critical for hemostasis and thrombosis, which plays an important role in Scott syndrome and has been confirmed by much research. However, few studies have investigated the association between TMEM16F and phagocytosis in ischemic stroke. In this study, a middle-cerebral-artery occlusion/reperfusion (MCAO/R) model was used in adult male Sprague-Dawley rats

Indexed as

AnimalsBrain IschemiaDisease Models, AnimalMaleMicrogliaNeuronsPhagocytosisPhospholipid Transfer ProteinsRatsRats, Sprague-DawleyReperfusion InjuryPhospholipid Transfer Proteinscerebral ischemiamicroglianeuronal cell deathphagocytosisTMEM16F

Identifiers

PMID32733436
PMCPMC7359929
OpenAlexW3039236706

What Socratic 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 Socratic graph.