Evidence map›Paper›PMID 32901466›Full record

ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2020

Knockout of VDAC1 in H9c2 Cells Promotes Oxidative Stress-Induced Cell Apoptosis through Decreased Mitochondrial Hexokinase II Binding and Enhanced Glycolytic Stress.

Meiying Yang, Jie Sun, David F Stowe, Emad Tajkhorshid, Wai-Meng Kwok, Amadou K S Camara

Open access · goldAbstract read
In one paragraph

Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Mitochondrial Kinase Signaling for Cardioprotection.International journal of molecular sciences · 2024
    Review
  7. Article
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  9. Review
  10. Article
  11. Article
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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

6 authors at 3 institutions in 2 countries.

Meiying YangDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA.
Jie SunDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA.
David F StoweDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA.
Emad TajkhorshidNIH Center for Macromolecular Modeling and Bioinformatics, Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana Champaign, Urbana, IL, USA.
Wai-Meng KwokDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA.
Amadou K S CamaraDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA, aksc@mcw.edu.
Medical College of Wisconsin · USMilwaukee VA Medical Center · USUniversity of Illinois Urbana-Champaign · US

Funding

Transformation of mitochondrial VDAC1 between protective and lethal statesR01HL131673 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI CAMARA, AMADOU K., KWOK, WAI-MENG · 2017 to 2020
$2.8M
Differential cardioprotection by mitochondrial Ca2+ sensitive potassium channelsI01BX002539 · VA · CLEMENT J. ZABLOCKI VA MEDICAL CENTER · PI STOWE, DAVID F · 2016 to 2019
–
BLRD VA I01 BX002539NHLBI NIH HHS R01 HL131673Veterans Administration BX002539
6 · The paper itself

Abstract

BACKGROUND/

aimsThe role of VDAC1, the most abundant mitochondrial outer membrane protein, in cell death depends on cell types and stimuli. Both silencing and upregulation of VDAC1 in various type of cancer cell lines can stimulate apoptosis. In contrast, in mouse embryonic stem (MES) cells and mouse embryonic fibroblasts (MEFs), the roles of VDAC1 knockout (VDAC1

methodsWe knocked out VDAC1 in this rat cardiomyoblast cell line with CRISPR-Cas9 genome editing technique to produce VDAC1

resultsWe found that under control conditions, VDAC1

conclusionOur results suggest that VDAC1

Indexed as

AnimalsApoptosisCell LineCell ProliferationCell SurvivalGene Knockout TechniquesGlycolysisHexokinaseMitochondriaMitochondrial MembranesMyocytes, CardiacOxidative StressRatsSignal Transductiontert-ButylhydroperoxideVoltage-Dependent Anion Channel 1Hexokinasetert-ButylhydroperoxideVdac1 protein, ratVoltage-Dependent Anion Channel 1VDAC1 knockout; Oxidative stress; Mitochondria-bound hexokinase II; Extracellular acidification; Cell death/apoptosis; Bax

Identifiers

PMID32901466
PMCPMC7898235
OpenAlexW3084774628

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.