Evidence map›Paper›PMID 38225236›Full record

ArticleCell death discovery2024

α-Ketoglutarate supplementation and NAD+ modulation enhance metabolic rewiring and radiosensitization in SLC25A1 inhibited cancer cells.

Kexu Xiang, Mikhail Kunin, Safa Larafa, Maike Busch, Nicole Dünker, Verena Jendrossek, Johann Matschke

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

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  10. Hyperpolarized MRI theranostics in cancer.Frontiers in oncology · 2025
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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 3 institutions in 2 countries.

Kexu XiangInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany.
Mikhail KuninInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany.
Safa LarafaInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany.ORCID http://orcid.org/0000-0001-5245-2373
Maike BuschCenter for Translational Neuro- and Behavioral Sciences, Institute of Anatomy II, Department of Neuroanatomy, Medical Faculty, University of Duisburg-Essen, 45147, Essen, Germany.
Nicole DünkerCenter for Translational Neuro- and Behavioral Sciences, Institute of Anatomy II, Department of Neuroanatomy, Medical Faculty, University of Duisburg-Essen, 45147, Essen, Germany.ORCID http://orcid.org/0000-0003-1273-0644
Verena JendrossekInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany.ORCID http://orcid.org/0000-0003-1058-2107
Johann MatschkeInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany. johann.matschke@uk-essen.de.ORCID http://orcid.org/0000-0003-4878-8741
University of Duisburg-Essen · DEEssen University Hospital · DEChongqing University · CN

Funding

Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research) 02NUK061BDeutsche Forschungsgemeinschaft (German Research Foundation) GRK1739/2Deutsche Forschungsgemeinschaft (German Research Foundation) MA 8970/1-1EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) 860245
6 · The paper itself

Abstract

Metabolic rewiring is the result of the increasing demands and proliferation of cancer cells, leading to changes in the biological activities and responses to treatment of cancer cells. The mitochondrial citrate transport protein SLC25A1 is involved in metabolic reprogramming offering a strategy to induce metabolic bottlenecks relevant to radiosensitization through the accumulation of the oncometabolite D-2-hydroxyglutarate (D-2HG) upon SLC25A1 inhibition (SLC25A1i). Previous studies have revealed the comparative effects of SLC25A1i or cell-permeable D-2HG (octyl-D-2HG) treatments on DNA damage induction and repair, as well as on energy metabolism and cellular function, which are crucial for the long-term survival of irradiated cells. Here, α-ketoglutarate (αKG), the precursor of D-2HG, potentiated the effects observed upon SLC25A1i on DNA damage repair, cell function and long-term survival in vitro and in vivo, rendering NCI-H460 cancer cells more vulnerable to ionizing radiation. However, αKG treatment alone had little effect on these phenotypes. In addition, supplementation with nicotinamide (NAM), a precursor of NAD (including NAD

Identifiers

PMID38225236
PMCPMC10789775
OpenAlexW4390876452

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.