Evidence map›Paper›PMID 36737819›Full record

ArticleJournal of translational medicine2023

VEGF-A enhances the cytotoxic function of CD4

Ziyi Chen, Meng Zhang, Yufeng Liu, Zhe Chen, Ling Wang, Wenjuan Wang, Jincheng Wang, Mingqian He, Bingyin Shi, Yue Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Cytotoxic CD4Signal transduction and targeted therapy · 2026
    Review
  4. Article
  5. Terminally differentiated cytotoxic CD4CNS neuroscience & therapeutics · 2024
    Article
  6. Review
  7. Review
  8. Review
  9. 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.

Ziyi Chen *Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Meng Zhang *Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Yufeng LiuMOE Key Lab for Intelligent Networks & Networks Security, School of Electronic and Information Engineering, Xi'an Jiaotong University, Xi'an, China.
Zhe ChenDepartment of Spine Surgery, Hong Hui Hospital, Xi'an Jiaotong University, Xi'an, China.
Ling WangDepartment of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Wenjuan WangDepartment of Hematology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Jincheng WangDepartment of Hematology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Mingqian HeDepartment of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Bingyin ShiDepartment of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. shibingy@126.com.
Yue WangDepartment of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. shelly1021@126.com.
First Affiliated Hospital of Xi'an Jiaotong University · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD4

methodsTo explore the potential regulators of the cytotoxicity of CD4 CTLs, bulk RNA and single-cell RNA sequencing (scRNA-seq), enzyme-linked immunosorbent assay, flow cytometry, quantitative PCR, and in-vitro stimulation and inhibition assays were performed.

resultsIn this study, we found that VEGF-A promoted the cytotoxicity of CD4 CTLs through scRNA-seq and flow cytometry. Regarding the specific VEGF receptor (R) involved, VEGF-R1/R2 signaling was activated in CD4 CTLs with increased cytotoxicity, and the VEGF-A effects were inhibited when anti-VEGF-R1/R2 neutralizing antibodies were applied. Mechanistically, VEGF-A treatment activated the AKT/mTOR pathway in CD4 CTLs, and the increases of cytotoxic molecules induced by VEGF-A were significantly reduced when the AKT/mTOR pathway was inhibited.

conclusionIn conclusion, VEGF-A enhances the cytotoxicity of CD4 CTLs through the VEGF-R1/VEGF-R2/AKT/mTOR pathway, providing insights for the development of novel treatments for disorders associated with CD4 CTLs.

Indexed as

Antineoplastic AgentsT-Lymphocytes, CytotoxicCD4-Positive T-LymphocytesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2Antineoplastic AgentsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2CD4 CTLsCD4+ cytotoxic T cellsGraves orbitopathymTORVEGF-AVEGF-R1VEGF-R2

Identifiers

PMID36737819
PMCPMC9896805
OpenAlexW4319080607

What OpenQuestion holds

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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.