Evidence map›Paper›PMID 31173576›Full record

ArticleAging2019

α-Ketoglutarate inhibits autophagy.

Elisa Elena Baracco, Francesca Castoldi, Sylvère Durand, David P Enot, Jelena Tadic, Katharina Kainz, Frank Madeo, Alexis Chery, Valentina Izzo, Maria Chiara Maiuri and 2 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  18. An Overview: The Diversified Role of Mitochondria in Cancer Metabolism.International journal of biological sciences · 2023
    Review
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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

12 authors at 8 institutions in 4 countries.

Elisa Elena Baracco *Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Descartes, Université Paris Diderot, "Metabolism, Cancer and Immunity", Paris 75006, France.
Francesca CastoldiCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Descartes, Université Paris Diderot, "Metabolism, Cancer and Immunity", Paris 75006, France.
Sylvère DurandCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Descartes, Université Paris Diderot, "Metabolism, Cancer and Immunity", Paris 75006, France.
David P EnotCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Descartes, Université Paris Diderot, "Metabolism, Cancer and Immunity", Paris 75006, France.
Jelena TadicInstitute of Molecular Biosciences, University of Graz, NAWI Graz, Graz, Austria.
Katharina KainzInstitute of Molecular Biosciences, University of Graz, NAWI Graz, Graz, Austria.
Frank MadeoInstitute of Molecular Biosciences, University of Graz, NAWI Graz, Graz, Austria.
Alexis CheryCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Descartes, Université Paris Diderot, "Metabolism, Cancer and Immunity", Paris 75006, France.
Valentina IzzoCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Descartes, Université Paris Diderot, "Metabolism, Cancer and Immunity", Paris 75006, France.
Maria Chiara MaiuriCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Descartes, Université Paris Diderot, "Metabolism, Cancer and Immunity", Paris 75006, France.
Federico PietrocolaCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Descartes, Université Paris Diderot, "Metabolism, Cancer and Immunity", Paris 75006, France.
Guido KroemerCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Descartes, Université Paris Diderot, "Metabolism, Cancer and Immunity", Paris 75006, France.
Institut Gustave Roussy · FRSorbonne Université · FRUniversity of Graz · ATCentre de Recherche des Cordeliers · FRInserm · FRInstitute for Research in Biomedicine · ESKarolinska Institutet · SENawi Graz · AT

Funding

Austrian Science Fund FWF P 29203Austrian Science Fund FWF P 31727Austrian Science Fund FWF W 1226
6 · The paper itself

Abstract

The metabolite α-ketoglutarate is membrane-impermeable, meaning that it is usually added to cells in the form of esters such as dimethyl -ketoglutarate (DMKG), trifluoromethylbenzyl α-ketoglutarate (TFMKG) and octyl α-ketoglutarate (O-KG). Once these compounds cross the plasma membrane, they are hydrolyzed by esterases to generate α-ketoglutarate, which remains trapped within cells. Here, we systematically compared DMKG, TFMKG and O-KG for their metabolic and functional effects. All three compounds similarly increased the intracellular levels of α-ketoglutarate, yet each of them had multiple effects on other metabolites that were not shared among the three agents, as determined by mass spectrometric metabolomics. While all three compounds reduced autophagy induced by culture in nutrient-free conditions, TFMKG and O-KG (but not DMKG) caused an increase in baseline autophagy in cells cultured in complete medium. O-KG (but neither DMKG nor TFMK) inhibited oxidative phosphorylation and exhibited cellular toxicity. Altogether, these results support the idea that intracellular α-ketoglutarate inhibits starvation-induced autophagy and that it has no direct respiration-inhibitory effect.

Indexed as

AutophagyCell Line, TumorHumansKetoglutaric AcidsMass SpectrometryOxidative Phosphorylationdimethyl alpha-ketoglutarateKetoglutaric Acidsacetyl CoAagingcell deathKrebs cyclemetabolomicsmitochondria

Identifiers

PMID31173576
PMCPMC6594794
OpenAlexW2953307224

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.