Evidence map›Paper›PMID 35783871›Full record

ArticleFrontiers in cardiovascular medicine2022

Deciphering Pro-angiogenic Transcription Factor Profiles in Hypoxic Human Endothelial Cells by Combined Bioinformatics and

Arne Schmidt, Maximilian Fuchs, Stevan D Stojanović, Chunguang Liang, Kevin Schmidt, Mira Jung, Ke Xiao, Jan Weusthoff, Annette Just, Angelika Pfanne and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 94% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

15 authors at 4 institutions in 1 country.

Arne SchmidtInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
Maximilian FuchsFraunhofer Cluster of Excellence Immune-Mediated Diseases (CIMD), Hanover, Germany.
Stevan D StojanovićInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
Chunguang LiangDepartment of Bioinformatics, Biocenter, University of Würzburg, Würzburg, Germany.
Kevin SchmidtInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
Mira JungInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
Ke XiaoInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
Jan WeusthoffInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
Annette JustInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
Angelika PfanneInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
Jörg H W DistlerDepartment of Internal Medicine 3 - Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander University (FAU) of Erlangen-Nürnberg, Erlangen, Germany.
Thomas DandekarDepartment of Bioinformatics, Biocenter, University of Würzburg, Würzburg, Germany.
Jan FiedlerInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
Thomas ThumInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
Meik KunzFraunhofer Cluster of Excellence Immune-Mediated Diseases (CIMD), Hanover, Germany.
Fraunhofer Institute for Toxicology and Experimental Medicine · DEMedizinische Hochschule Hannover · DEUniversity of Würzburg · DEUniversitätsklinikum Erlangen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Constant supply of oxygen is crucial for multicellular tissue homeostasis and energy metabolism in cardiac tissue. As a first response to acute hypoxia, endothelial cells (ECs) promote recruitment and adherence of immune cells to the dysbalanced EC barrier by releasing inflammatory mediators and growth factors, whereas chronic hypoxia leads to the activation of a transcription factor (TF) battery, that potently induces expression of growth factors and cytokines including platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF). We report a hypoxia-minded, targeted bioinformatics approach aiming to identify and validate TFs that regulate angiogenic signaling. Results: A comprehensive RNA-Seq dataset derived from human ECs subjected to normoxic or hypoxic conditions was selected to identify significantly regulated genes based on (i) fold change (normoxia vs. hypoxia) and (ii) relative abundancy. Transcriptional regulation of this gene set was confirmed Conclusion: By detailed

Indexed as

angiogenesisendothelialhypoxiapromoter profilingsignalingtranscription factor

Identifiers

PMID35783871
PMCPMC9247153
OpenAlexW4283026272

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.