Evidence map›Paper›PMID 35181679›Full record

ArticleNature communications2022

ATF-4 and hydrogen sulfide signalling mediate longevity in response to inhibition of translation or mTORC1.

Cyril Statzer, Jin Meng, Richard Venz, Monet Bland, Stacey Robida-Stubbs, Krina Patel, Dunja Petrovic, Raffaella Emsley, Pengpeng Liu, Ianessa Morantte and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
8.2field-weighted citation impact, top 1% 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

64 citing papers in PubMed, 100 citations in OpenAlex.

  1. Review
  2. Article
  3. Vitamin BNature communications · 2026
    Article
  4. Article
  5. Suppression rather than activation of the integrated stress response (GCN2-ATF4) pathway extends lifespan in the fly.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Cystathionine γ-lyase is a major regulator of cognitive function through neurotrophin signaling and neurogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Article
  14. Article
  15. Vitamin BResearch square · 2025
    Article
  16. Article
  17. Targeting macro- and micro-nutrient regulation of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  18. Article
  19. Article
  20. Article

4 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

16 authors at 7 institutions in 3 countries.

Cyril Statzer *Eidgenössische Technische Hochschule Zürich, Department of Health Sciences and Technology, Institute of Translational Medicine, Schwerzenbach, Switzerland.
Jin Meng *Department of Genetics, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-1347-9730
Richard VenzEidgenössische Technische Hochschule Zürich, Department of Health Sciences and Technology, Institute of Translational Medicine, Schwerzenbach, Switzerland.
Monet BlandDepartment of Genetics, Harvard Medical School, Boston, MA, USA.
Stacey Robida-StubbsDepartment of Genetics, Harvard Medical School, Boston, MA, USA.
Krina PatelDepartment of Genetics, Harvard Medical School, Boston, MA, USA.
Dunja PetrovicLeibniz-Institut für Analytische Wissenschaften-ISAS-e.V., Dortmund, Germany.
Raffaella EmsleyDepartment of Vascular Surgery, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland.
Pengpeng LiuDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.
Ianessa MorantteDepartment of Genetics and Complex Diseases, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA, USA.
Cole HaynesDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.ORCID http://orcid.org/0000-0003-2110-5648
William B MairDepartment of Genetics and Complex Diseases, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA, USA.ORCID http://orcid.org/0000-0002-0661-1342
Alban LongchampDepartment of Vascular Surgery, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland.ORCID http://orcid.org/0000-0002-1743-4935
Milos R FilipovicLeibniz-Institut für Analytische Wissenschaften-ISAS-e.V., Dortmund, Germany.
T Keith BlackwellDepartment of Genetics, Harvard Medical School, Boston, MA, USA. keith.blackwell@joslin.harvard.edu.ORCID http://orcid.org/0000-0003-3763-9134
Collin Y EwaldEidgenössische Technische Hochschule Zürich, Department of Health Sciences and Technology, Institute of Translational Medicine, Schwerzenbach, Switzerland. collin-ewald@ethz.ch.ORCID http://orcid.org/0000-0003-1166-4171
Joslin Diabetes Center · USETH Zurich · CHHarvard University · USLeibniz Institute for Analytical Sciences - ISAS · DEUniversity Hospital of Lausanne · CHUniversity of Massachusetts Chan Medical School · USBoard of the Swiss Federal Institutes of Technology · CH

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Signaling mechanisms that detect stress and maintain homeostasis - Research Supplement to Promote Diversity in Health-Related ResearchR35GM122610 · NIGMS · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 2017 to 2025
$4.7M
Uncovering Conserved Lipid Homeostasis Mechanisms that Mediate Longevity after Germ Cell Loss in C. ElegansR01AG054215 · NIA · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 2017 to 2026
$3.9M
Orchestra: A high performance biomedical supercomputing collaborativeS10RR028832 · NCRR · HARVARD MEDICAL SCHOOL · PI DANUSER, GAUDENZ · 2010 to 2010
$3.7M
NCRR NIH HHS S10 RR028832NIA NIH HHS R01 AG054215NIDDK NIH HHS P30 DK036836NIGMS NIH HHS R35 GM122610NIH HHS P40 OD010440
6 · The paper itself

Abstract

Inhibition of the master growth regulator mTORC1 (mechanistic target of rapamycin complex 1) slows ageing across phyla, in part by reducing protein synthesis. Various stresses globally suppress protein synthesis through the integrated stress response (ISR), resulting in preferential translation of the transcription factor ATF-4. Here we show in C. elegans that inhibition of translation or mTORC1 increases ATF-4 expression, and that ATF-4 mediates longevity under these conditions independently of ISR signalling. ATF-4 promotes longevity by activating canonical anti-ageing mechanisms, but also by elevating expression of the transsulfuration enzyme CTH-2 to increase hydrogen sulfide (H

Indexed as

Activating Transcription Factor 4AnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsHydrogen SulfideLongevityMechanistic Target of Rapamycin Complex 1Signal TransductionActivating Transcription Factor 4Caenorhabditis elegans ProteinsHydrogen SulfideMechanistic Target of Rapamycin Complex 1

Identifiers

PMID35181679
PMCPMC8857226
OpenAlexW4212893161

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.