Evidence map›Paper›PMID 36442394›Full record

ArticleRedox biology2022

Mitochondria-originated redox signalling regulates KLF-1 to promote longevity in Caenorhabditis elegans.

Johannes Cw Hermeling, Marija Herholz, Linda Baumann, Estela Cepeda Cores, Aleksandra Zečić, Thorsten Hoppe, Jan Riemer, Aleksandra Trifunovic

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. PeerJ · 2025
    Article
  6. Redox regulation in lifespan determination.The Journal of biological chemistry · 2024
    Review
  7. Icariin Improves Stress Resistance and Extends Lifespan inInternational journal of molecular sciences · 2023
    Article
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

8 authors at 1 institution in 1 country.

Johannes Cw HermelingCologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated Diseases (CECAD), Germany; Institute for Mitochondrial Diseases and Ageing, Medical Faculty, University of Cologne, Cologne, D-50931, Germany.
Marija HerholzCologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated Diseases (CECAD), Germany; Institute for Mitochondrial Diseases and Ageing, Medical Faculty, University of Cologne, Cologne, D-50931, Germany.
Linda BaumannCologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated Diseases (CECAD), Germany; Institute for Mitochondrial Diseases and Ageing, Medical Faculty, University of Cologne, Cologne, D-50931, Germany.
Estela Cepeda CoresCologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated Diseases (CECAD), Germany; Institute for Mitochondrial Diseases and Ageing, Medical Faculty, University of Cologne, Cologne, D-50931, Germany.
Aleksandra ZečićCologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated Diseases (CECAD), Germany; Institute for Mitochondrial Diseases and Ageing, Medical Faculty, University of Cologne, Cologne, D-50931, Germany.
Thorsten HoppeCologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated Diseases (CECAD), Germany; Center for Molecular Medicine Cologne (CMMC), Cologne, D-50931, Germany; Institute for Genetics, University of Cologne, Cologne, D-50674, Germany.
Jan RiemerCologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated Diseases (CECAD), Germany; Institute for Biochemistry, University of Cologne, Cologne, D-50931, Germany.
Aleksandra TrifunovicCologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated Diseases (CECAD), Germany; Institute for Mitochondrial Diseases and Ageing, Medical Faculty, University of Cologne, Cologne, D-50931, Germany; Center for Molecular Medicine Cologne (CMMC), Cologne, D-50931, Germany. Electronic address: aleksandra.trifunovic@uk-koeln.de.
University of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alternations of redox metabolism have been associated with the extension of lifespan in roundworm Caenorhabditis elegans, caused by moderate mitochondrial dysfunction, although the underlying signalling cascades are largely unknown. Previously, we identified transcriptional factor Krüppel-like factor-1 (KLF-1) as the main regulator of cytoprotective longevity-assurance pathways in the C. elegans long-lived mitochondrial mutants. Here, we show that KLF-1 translocation to the nucleus and the activation of the signalling cascade is dependent on the mitochondria-derived hydrogen peroxide (H

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsAnimalsHydrogen PeroxideKruppel-Like Transcription FactorsLongevityMitochondriaOxidation-ReductionCaenorhabditis elegans ProteinsHydrogen PeroxideKlf-1 protein, C elegansKruppel-Like Transcription Factors

Identifiers

PMID36442394
PMCPMC9709155
OpenAlexW4309763228

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.