Evidence map›Paper›PMID 27140632›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Roles for ROS and hydrogen sulfide in the longevity response to germline loss in Caenorhabditis elegans.

Yuehua Wei, Cynthia Kenyon

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. bioRxiv : the preprint server for biology · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Iron-deplete diet enhancesbioRxiv : the preprint server for biology · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Redox regulation in lifespan determination.The Journal of biological chemistry · 2024
    Review
  19. Review
  20. Article

20 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Yuehua WeiDepartment of Biochemistry and Biophysics, University of California, San Francisco, CA 94158.
Cynthia KenyonDepartment of Biochemistry and Biophysics, University of California, San Francisco, CA 94158 cynthia@calicolabs.com.
University of California, San Francisco · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
Signals from the reproductive system that regulate aging in C. elegansR01AG032435 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LI, HAO · 2009 to 2018
$3.3M
NIA NIH HHS R01 AG032435NIH HHS P40 OD010440
6 · The paper itself

Abstract

In Caenorhabditis elegans, removing germ cells slows aging and extends life. Here we show that transcription factors that extend life and confer protection to age-related protein-aggregation toxicity are activated early in adulthood in response to a burst of reactive oxygen species (ROS) and a shift in sulfur metabolism. Germline loss triggers H2S production, mitochondrial biogenesis, and a dynamic pattern of ROS in specific somatic tissues. A cytoskeletal protein, KRI-1, plays a key role in the generation of H2S and ROS. These kri-1-dependent redox species, in turn, promote life extension by activating SKN-1/Nrf2 and the mitochondrial unfolded-protein response, respectively. Both H2S and, remarkably, kri-1-dependent ROS are required for the life extension produced by low levels of the superoxide-generator paraquat and by a mutation that inhibits respiration. Together our findings link reproductive signaling to mitochondria and define an inducible, kri-1-dependent redox-signaling module that can be invoked in different contexts to extend life and counteract proteotoxicity.

Indexed as

AgingActive Transport, Cell NucleusAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA-Binding ProteinsGerm CellsHydrogen SulfideIntracellular Signaling Peptides and ProteinsLongevityMitochondrial DynamicsOrganelle BiogenesisOxidation-ReductionReactive Oxygen SpeciesSignal TransductionTranscription FactorsCaenorhabditis elegans ProteinsDNA-Binding ProteinsHydrogen SulfideIntracellular Signaling Peptides and ProteinsKRI-1 protein, C elegansReactive Oxygen Speciesskn-1 protein, C elegansTranscription FactorsAβhormesisKRIT1Nrf2SKN-1

Identifiers

PMID27140632
PMCPMC4878494
OpenAlexW2345997946

What OpenQuestion holds

Textmetadata
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.