Evidence map›Paper›PMID 35297148›Full record

ArticleEMBO reports2022

CEST-2.2 overexpression alters lipid metabolism and extends longevity of mitochondrial mutants.

Antonia Piazzesi, Yiru Wang, Joshua Jackson, Lena Wischhof, Viktoria Zeisler-Diehl, Enzo Scifo, Ina Oganezova, Thorben Hoffmann, Pablo Gómez Martín, Fabio Bertan and 9 more

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

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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

19 authors at 3 institutions in 2 countries.

Antonia Piazzesi *German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.ORCID 0000-0002-7591-6473
Yiru Wang *German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.ORCID 0000-0002-6522-9995
Joshua Jackson *German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.ORCID 0000-0002-3515-5593
Lena WischhofGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.ORCID 0000-0002-2203-408X
Viktoria Zeisler-DiehlInstitute of Cellular and Molecular Botany (IZMB), University of Bonn, Bonn, Germany.
Enzo ScifoGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.ORCID 0000-0002-0450-6573
Ina OganezovaGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.ORCID 0000-0001-8672-8497
Thorben HoffmannGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.ORCID 0000-0001-5532-6153
Pablo Gómez MartínGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Fabio BertanGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Chester J J WrobelBoyce Thompson Institute and Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY, USA.
Frank C SchroederBoyce Thompson Institute and Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY, USA.
Dan EhningerGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Kristian HändlerGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Joachim L SchultzeGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Lukas SchreiberInstitute of Cellular and Molecular Botany (IZMB), University of Bonn, Bonn, Germany.ORCID 0000-0001-7003-9929
Gerhild van Echten-DeckertLIMES Institute for Membrane Biology and Lipid Biochemistry, University of Bonn, Bonn, Germany.ORCID 0000-0002-2816-7852
Pierluigi NicoteraGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.ORCID 0000-0003-1175-7466
Daniele BanoGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.ORCID 0000-0002-9617-5504
German Center for Neurodegenerative Diseases · DEUniversity of Bonn · DECornell University · US

Funding

Small molecule signaling in C. elegansR35GM131877 · NIGMS · BOYCE THOMPSON INST FOR PLANT RESEARCH · PI Frank Clemens Schroeder · 2019 to 2026
$5.0M
NIGMS NIH HHS R35 GM131877
6 · The paper itself

Abstract

Mitochondrial dysfunction can either extend or decrease Caenorhabditis elegans lifespan, depending on whether transcriptionally regulated responses can elicit durable stress adaptation to otherwise detrimental lesions. Here, we test the hypothesis that enhanced metabolic flexibility is sufficient to circumvent bioenergetic abnormalities associated with the phenotypic threshold effect, thereby transforming short-lived mitochondrial mutants into long-lived ones. We find that CEST-2.2, a carboxylesterase mainly localizes in the intestine, may stimulate the survival of mitochondrial deficient animals. We report that genetic manipulation of cest-2.2 expression has a minor lifespan impact on wild-type nematodes, whereas its overexpression markedly extends the lifespan of complex I-deficient gas-1(fc21) mutants. We profile the transcriptome and lipidome of cest-2.2 overexpressing animals and show that CEST-2.2 stimulates lipid metabolism and fatty acid beta-oxidation, thereby enhancing mitochondrial respiratory capacity through complex II and LET-721/ETFDH, despite the inherited genetic lesion of complex I. Together, our findings unveil a metabolic pathway that, through the tissue-specific mobilization of lipid deposits, may influence the longevity of mitochondrial mutant C. elegans.

Indexed as

Caenorhabditis elegans ProteinsLongevityAnimalsCaenorhabditis elegansLipid MetabolismMitochondriaCaenorhabditis elegans ProteinsCaenorhabditis eleganscarboxylesterase CEST-2.2epigeneticslipid metabolismmitochondria

Identifiers

PMID35297148
PMCPMC9066074
OpenAlexW4221012100

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.