Evidence map›Paper›PMID 40235395›Full record

ArticleJournal of cell science2025

Approaches to reduce succinate accumulation by restoration of succinate dehydrogenase activity in cultured adrenal cells.

Fatimah Al Khazal, Leili Rahimi, Fan Feng, Nicole A Becker, Clifford D Folmes, Judith Favier, L James Maher

Erratum issuedAbstract read
In one paragraph

Article in Journal of cell science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Fatimah Al KhazalDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine and Science, Rochester, MN 55905, USA.
Leili RahimiDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine and Science, Rochester, MN 55905, USA.
Fan FengDepartment of Biochemistry and Molecular Biology, Department of Cardiovascular Medicine, Mayo Clinic College of Medicine and Science, Scottsdale, AZ 85259, USA.
Nicole A BeckerDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine and Science, Rochester, MN 55905, USA.
Clifford D FolmesDepartment of Biochemistry and Molecular Biology, Department of Cardiovascular Medicine, Mayo Clinic College of Medicine and Science, Scottsdale, AZ 85259, USA.
Judith FavierInserm, Centre de recherche des Cordeliers, Université Paris-Cité, Sorbonne Université, Equipe Labellisée Ligue contre le Cancer, 75006, Paris, France.
L James MaherDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine and Science, Rochester, MN 55905, USA.ORCID 0000-0002-5043-6422

Funding

Metabolic reprogramming in pluripotent induction and cardiac lineage specificatioR00HL121079 · NHLBI · MAYO CLINIC ARIZONA · PI FOLMES, CLIFFORD D · 2017 to 2019
$747k
Genome-wide synthetic lethal screening for vulnerabilities in a cell model of succinate dehydrogenase-loss paragangliomaR21CA266999 · NCI · MAYO CLINIC ROCHESTER · PI MAHER, LOUIS JAMES · 2023 to 2024
$400k
Metabolic reprogramming in pluripotent induction and cardiac lineage specificatioK99HL121079 · NHLBI · MAYO CLINIC ROCHESTER · PI FOLMES, CLIFFORD D · 2014 to 2015
$279k
Mayo ClinicMayo Clinic Division of Endocrinology and MetabolismNCI NIH HHS R21 CA266999NHLBI NIH HHS HL121079NHLBI NIH HHS K99 HL121079NHLBI NIH HHS R00 HL121079NIGMS NIH HHS R21CA266999NIH HHS R21CA266999Paradifference foundationParadifference Foundation HL121079
6 · The paper itself

Abstract

The rare human neuroendocrine tumors pheochromocytoma and paraganglioma (PPGL) can result from loss of mitochondrial succinate dehydrogenase. The resulting succinate accumulation is tumorigenic in certain neuroendocrine cells. Here, we explore two theoretical approaches to mitigate tumorigenic succinate accumulation in a cell culture model of PPGL. We first study a gene replacement strategy using transposition technology, and conclude that many of the changes in mitochondrial morphology, oxidative cell metabolism and succinate accumulation can be reversed by this process. We then investigate whether riboflavin supplementation has the potential to rescue succinate dehydrogenase activity in the intact SDHA catalytic subunit to suppress succinate accumulation even in the absence of SDHB. We show that this latter strategy is not successful.

Indexed as

Adrenal GlandsSuccinate DehydrogenaseSuccinic AcidAdrenal Gland NeoplasmsCell Line, TumorCells, CulturedElectron Transport Complex IIHumansMitochondriaParagangliomaPheochromocytomaRiboflavinElectron Transport Complex IIRiboflavinSDHA protein, humanSuccinate DehydrogenaseSuccinic AcidParagangliomaPheochromocytomaRiboflavinSuccinate dehydrogenase

Identifiers

PMID40235395
PMCPMC12136175

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.