Evidence map›Paper›PMID 31000420›Full record

ArticleEBioMedicine2019

Endothelial FAM3A positively regulates post-ischaemic angiogenesis.

Wenjing Xu, Minglu Liang, Yanqing Zhang, Kai Huang, Cheng Wang

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  16. CREB Coactivator CRTC2 Plays a Crucial Role in Endothelial Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  17. Article
  18. Review
  19. 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

5 authors at 1 institution in 1 country.

Wenjing XuClinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Minglu LiangClinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yanqing ZhangClinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Kai HuangClinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Cheng WangClinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Rheumatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address: cwangunion@hust.edu.cn.
Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAngiogenesis improves reperfusion to the ischaemic tissue after vascular obstruction. The underlying molecular mechanisms of post-ischaemic angiogenesis are not clear. FAM3A belongs to the family with sequence similarity 3 (FAM3) genes, but its biological function in endothelial cells in regards to vascular diseases is not well understood.

methodsGain- and loss-of-function methods by adenovirus or associated-adenovirus (AAV) in different models were applied to investigate the effects of FAM3A on endothelial angiogenesis. Endothelial angiogenesis was analysed by tube formation, migration and proliferation in vitro, and the blood flow and capillary density in a hind limb ischaemic model in vivo.

findingsEndothelial FAM3A expression is downregulated under hypoxic conditions. Overexpression of FAM3A promotes, but depletion of FAM3A suppresses, endothelial tube formation, proliferation and migration. Utilizing the mouse hind limb ischaemia model, we also observe that FAM3A overexpression can improve blood perfusion and increase capillary density, whereas FAM3A knockdown has the opposite effects. Mechanistically, mitochondrial FAM3A increases adenosine triphosphate (ATP) production and secretion; ATP binds to P2 receptors and then upregulates cytosolic free Ca

interpretationIn summary, our data demonstrate that FAM3A positively regulates angiogenesis through activation of VEGFA transcription, suggesting that FAM3A may constitute a novel molecular therapeutic target for ischaemic vascular disease.

Indexed as

Gene Expression RegulationAdenosine TriphosphateAnimalsBiomarkersCalciumCalcium SignalingCell LineCyclic AMP Response Element-Binding ProteinCytokinesDisease Models, AnimalEndothelial CellsGene Knockdown TechniquesHumansImmunohistochemistryIschemiaMaleAdenosine TriphosphateBiomarkersCalciumCyclic AMP Response Element-Binding ProteinCytokinesFAM3A protein, mouseVascular Endothelial Growth Factor AVEGFA protein, humanAngiogenesisATPCREBFAM3ATranscriptionVEGF-A

Identifiers

PMID31000420
PMCPMC6562148
OpenAlexW2939473164

What OpenQuestion 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 OpenQuestion graph.