Evidence map›Paper›PMID 39532882›Full record

ArticleNature communications2024

HSF-1 promotes longevity through ubiquilin-1-dependent mitochondrial network remodelling.

Annmary Paul Erinjeri, Xunyan Wang, Rhianna Williams, Riccardo Zenezini Chiozzi, Konstantinos Thalassinos, Johnathan Labbadia

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. More than the 'master regulator of cytosolic proteostasis': new roles for HSF1 in promoting tissue health.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Genome-Wide Identification, Expression Analysis ofPlants (Basel, Switzerland) · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. A default silencing mechanism restrains stress-induced genes inbioRxiv : the preprint server for biology · 2025
    Article
  12. ThebioRxiv : the preprint server for biology · 2025
    Article
  13. Article
  14. HSPBiomedicines · 2025
    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

6 authors.

Annmary Paul ErinjeriInstitute of Healthy Ageing, Department of Genetics, Evolution and Environment, Division of Biosciences, University College London, London, UK.ORCID 0000-0002-1427-5342
Xunyan WangInstitute of Healthy Ageing, Department of Genetics, Evolution and Environment, Division of Biosciences, University College London, London, UK.
Rhianna WilliamsInstitute of Healthy Ageing, Department of Genetics, Evolution and Environment, Division of Biosciences, University College London, London, UK.
Riccardo Zenezini ChiozziInstitute of Structural and Molecular Biology, Division of Biosciences, University College London, London, UK.ORCID 0000-0003-3904-5532
Konstantinos ThalassinosInstitute of Structural and Molecular Biology, Division of Biosciences, University College London, London, UK.ORCID 0000-0001-5072-8428
Johnathan LabbadiaInstitute of Healthy Ageing, Department of Genetics, Evolution and Environment, Division of Biosciences, University College London, London, UK. j.labbadia@ucl.ac.uk.ORCID 0000-0001-9625-2816

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440RCUK | Biotechnology and Biological Sciences Research Council (BBSRC) BB/T013273/1Wellcome TrustWellcome Trust (Wellcome) 209250/Z/17/ZWellcome Trust (Wellcome) 221521/Z/20/Z
6 · The paper itself

Abstract

Increased activity of the heat shock factor, HSF-1, suppresses proteotoxicity and enhances longevity. However, the precise mechanisms by which HSF-1 promotes lifespan are unclear. Using an RNAi screen, we identify ubiquilin-1 (ubql-1) as an essential mediator of lifespan extension in worms overexpressing hsf-1. We find that hsf-1 overexpression leads to transcriptional downregulation of all components of the CDC-48-UFD-1-NPL-4 complex, which is central to both endoplasmic reticulum and mitochondria associated protein degradation, and that this is complemented by UBQL-1-dependent turnover of NPL-4.1. As a consequence, mitochondrial network dynamics are altered, leading to increased lifespan. Together, our data establish that HSF-1 mediates lifespan extension through mitochondrial network adaptations that occur in response to down-tuning of components associated with organellar protein degradation pathways.

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsLongevityMitochondriaTranscription FactorsAnimalsEndoplasmic ReticulumRNA InterferenceCaenorhabditis elegans ProteinsTranscription Factors

Identifiers

PMID39532882
PMCPMC11557981

What OpenQuestion holds

Textmetadata
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.