Evidence map›Paper›PMID 33001475›Full record

ArticleThe EMBO journal2020

Nox4 regulates InsP

Matteo Beretta, Celio Xc Santos, Chris Molenaar, Anne D Hafstad, Chris Cj Miller, Aram Revazian, Kai Betteridge, Katrin Schröder, Katrin Streckfuß-Bömeke, James H Doroshow and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
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  5. Redox signals and oxidative stress in the control of mitochondrial protein import.Protein science : a publication of the Protein Society · 2026
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  14. Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 7 institutions in 6 countries.

Matteo BerettaSchool of Cardiovascular Medicine & Sciences, King's College London British Heart Foundation Centre, London, UK.
Celio Xc SantosSchool of Cardiovascular Medicine & Sciences, King's College London British Heart Foundation Centre, London, UK.
Chris MolenaarSchool of Cardiovascular Medicine & Sciences, King's College London British Heart Foundation Centre, London, UK.
Anne D HafstadSchool of Cardiovascular Medicine & Sciences, King's College London British Heart Foundation Centre, London, UK.
Chris Cj MillerDepartment of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.ORCID 0000-0002-5130-1845
Aram RevazianInstitute for Cardiovascular Physiology, Georg August University Göttingen, Göttingen, Germany.
Kai BetteridgeSchool of Cardiovascular Medicine & Sciences, King's College London British Heart Foundation Centre, London, UK.
Katrin SchröderInstitute for Cardiovascular Physiology, Goethe-University Frankfurt, Frankfurt am Main, Germany.ORCID 0000-0002-3099-526X
Katrin Streckfuß-BömekeDepartment of Cardiology and Pneumology, Universitätsmedizin Göttingen, Göttingen, Germany.ORCID 0000-0001-5137-7228
James H DoroshowDivision of Cancer Treatment and Diagnosis, National Cancer Institute, NIH, Bethesda, MD, USA.
Roland A FleckCentre for Ultrastructural Imaging, King's College London, London, UK.
Tsung-Ping SuCellular Pathobiology Section, National Institute on Drug Abuse, NIH, Baltimore, MD, USA.
Vsevolod V BelousovInstitute for Cardiovascular Physiology, Georg August University Göttingen, Göttingen, Germany.
Maddy ParsonsKing's College London British Heart Foundation Centre, Randall Centre of Cell and Molecular Biophysics, London, UK.ORCID 0000-0002-2021-8379
Ajay M ShahSchool of Cardiovascular Medicine & Sciences, King's College London British Heart Foundation Centre, London, UK.ORCID 0000-0002-6547-0631
King's College London · GBGoethe University Frankfurt · DENational Cancer Institute · MYNational Institute on Drug Abuse · USPirogov Russian National Research Medical University · RUUniversitätsmedizin Göttingen · DEUniversity of Göttingen · DE

Funding

Arthritis Research UK ARUK-EG2013B-1British Heart Foundation RG/20/3/34823British Heart Foundation (BHF) CH/1999001/11735British Heart Foundation (BHF) RG/13/11/30384DFG IRTG 1816Fondation Leducq 17CVD04National Institute for Health Research (NIHR) IS-BRC-1215-20006Russian Science Foundation (RSF) 17-14-01086
6 · The paper itself

Abstract

Cells subjected to environmental stresses undergo regulated cell death (RCD) when homeostatic programs fail to maintain viability. A major mechanism of RCD is the excessive calcium loading of mitochondria and consequent triggering of the mitochondrial permeability transition (mPT), which is especially important in post-mitotic cells such as cardiomyocytes and neurons. Here, we show that stress-induced upregulation of the ROS-generating protein Nox4 at the ER-mitochondria contact sites (MAMs) is a pro-survival mechanism that inhibits calcium transfer through InsP

Indexed as

Calcium SignalingAnimalsCalciumCell SurvivalInositol 1,4,5-Trisphosphate ReceptorsMitochondria, HeartMyocardial Reperfusion InjuryMyocytes, CardiacNADPH Oxidase 4Oxidative StressRatsCalciumInositol 1,4,5-Trisphosphate ReceptorsNADPH Oxidase 4Nox4 protein, mouseNox4 protein, ratcalcium signalingcell deathInsP3 receptormitochondria-associated membraneNADPH oxidase-4

Identifiers

PMID33001475
PMCPMC7527947
OpenAlexW3048177327

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.