Evidence map›Paper›PMID 34523215›Full record

ArticleJournal of cellular and molecular medicine2021

Hypoxia-inducible factor 1-alpha acts as a bridge factor for crosstalk between ERK1/2 and caspases in hypoxia-induced apoptosis of cementoblasts.

Jiawen Yong, Julia von Bremen, Sabine Groeger, Gisela Ruiz-Heiland, Sabine Ruf

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 25 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

5 authors at 1 institution in 1 country.

Jiawen YongDepartment of Orthodontics, Faculty of Medicine, Justus Liebig University Giessen, Giessen, Germany.ORCID 0000-0002-3021-075X
Julia von BremenDepartment of Orthodontics, Faculty of Medicine, Justus Liebig University Giessen, Giessen, Germany.
Sabine GroegerDepartment of Periodontics, Faculty of Medicine, Justus Liebig University Giessen, Giessen, Germany.
Gisela Ruiz-HeilandDepartment of Orthodontics, Faculty of Medicine, Justus Liebig University Giessen, Giessen, Germany.
Sabine RufDepartment of Orthodontics, Faculty of Medicine, Justus Liebig University Giessen, Giessen, Germany.
Justus-Liebig-Universität Gießen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia-induced apoptosis of cementoblasts (OCCM-30) may be harmful to orthodontic treatment. Hypoxia-inducible factor 1-alpha (HIF-1α) mediates the biological effects during hypoxia. Little is known about the survival mechanism capable to counteract cementoblast apoptosis. We aimed to investigate the potential roles of HIF-1α, as well as the protein-protein interactions with ERK1/2, using an in-vitro model of chemical-mimicked hypoxia and adipokines. Here, OCCM-30 were co-stimulated with resistin, visfatin or ghrelin under CoCl

Indexed as

AdipokinesAnimalsApoptosisCaspasesCell HypoxiaCobaltDental CementumGene ExpressionHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NecrosisProtein Kinase InhibitorsSignal TransductionAdipokinesCaspasesCobaltcobaltous chlorideHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMapk1 protein, mouseMapk3 protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Protein Kinase Inhibitorsadipokinesapoptosiscementoblastscobalt (II) chloridehypoxia

Identifiers

PMID34523215
PMCPMC8505834
OpenAlexW3199576158

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.