Evidence map›Paper›PMID 30781698›Full record

ArticleCells2019

Chronic Hypoxia Enhances β-Oxidation-Dependent Electron Transport via Electron Transferring Flavoproteins.

Dominik C Fuhrmann, Catherine Olesch, Nina Kurrle, Frank Schnütgen, Sven Zukunft, Ingrid Fleming, Bernhard Brüne

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. 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
1.1field-weighted citation impact, top 23% 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, 24 citations in OpenAlex.

  1. 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

7 authors at 1 institution in 1 country.

Dominik C FuhrmannInstitute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany.
Catherine OleschInstitute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany.
Nina KurrleDepartment of Medicine, Hematology/Oncology, Goethe-University Frankfurt, 60590 Frankfurt, Germany.
Frank SchnütgenDepartment of Medicine, Hematology/Oncology, Goethe-University Frankfurt, 60590 Frankfurt, Germany.
Sven ZukunftInstitute for Vascular Signaling, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany.
Ingrid FlemingInstitute for Vascular Signaling, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany.
Bernhard BrüneInstitute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany. b.bruene@biochem.uni-frankfurt.de.ORCID 0000-0001-8237-2841
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia poses a stress to cells and decreases mitochondrial respiration, in part by electron transport chain (ETC) complex reorganization. While metabolism under acute hypoxia is well characterized, alterations under chronic hypoxia largely remain unexplored. We followed oxygen consumption rates in THP-1 monocytes during acute (16 h) and chronic (72 h) hypoxia, compared to normoxia, to analyze the electron flows associated with glycolysis, glutamine, and fatty acid oxidation. Oxygen consumption under acute hypoxia predominantly demanded pyruvate, while under chronic hypoxia, fatty acid- and glutamine-oxidation dominated. Chronic hypoxia also elevated electron-transferring flavoproteins (ETF), and the knockdown of ETF⁻ubiquinone oxidoreductase lowered mitochondrial respiration under chronic hypoxia. Metabolomics revealed an increase in citrate under chronic hypoxia, which implied glutamine processing to α-ketoglutarate and citrate. Expression regulation of enzymes involved in this metabolic shunting corroborated this assumption. Moreover, the expression of acetyl-CoA carboxylase 1 increased, thus pointing to fatty acid synthesis under chronic hypoxia. Cells lacking complex I, which experienced a markedly impaired respiration under normoxia, also shifted their metabolism to fatty acid-dependent synthesis and usage. Taken together, we provide evidence that chronic hypoxia fuels the ETC via ETFs, increasing fatty acid production and consumption via the glutamine-citrate-fatty acid axis.

Indexed as

Cell HypoxiaCell RespirationElectron-Transferring FlavoproteinsElectron TransportElectron Transport Complex IFatty AcidsGlutamineHumansIron-Sulfur ProteinsMembrane Potential, MitochondrialMembrane ProteinsMitochondriaModels, BiologicalOxidation-ReductionOxidoreductases Acting on CH-NH Group DonorsOxygen Consumptionelectron-transferring-flavoprotein dehydrogenaseElectron-Transferring FlavoproteinsElectron Transport Complex IFatty AcidsGlutamineIron-Sulfur ProteinsMembrane ProteinsOxidoreductases Acting on CH-NH Group DonorsTMEM126B protein, humancomplex Ielectron transport chainfatty acidsglutaminemitochondriamonocytesTMEM126B

Identifiers

PMID30781698
PMCPMC6406996
OpenAlexW2911747707

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.