Evidence map›Paper›PMID 36342845›Full record

ReviewGenetics2022

Mitochondrial dysfunction, aging, and the mitochondrial unfolded protein response in Caenorhabditis elegans.

Cole M Haynes, Siegfried Hekimi

Open access · bronzeAbstract readReview
In one paragraph

Review in Genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. HSP60 and HSP10 depletion provoke distinct biological responses.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. UPRNature metabolism · 2025
    Article
  19. Review
  20. Modeling Host-Pathogen Interactions inInternational journal of molecular sciences · 2024
    Review
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 2 institutions in 2 countries.

Cole M HaynesMolecular, Cell and Cancer Biology, UMass-Chan Medical School, Worcester, MA 01655, USA.ORCID 0000-0003-2110-5648
Siegfried HekimiDepartment of Biology, McGill University, Montreal, QC H3A 0G4, Canada.ORCID 0000-0002-3592-5711
McGill University · CAUniversity of Massachusetts Chan Medical School · US

Funding

Coordinated Repair and Regeneration of Defective MitochondriaR37AG047182 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Cole M Haynes · 2020 to 2026
$3.2M
Coordinating mitochondrial network expansion and longevity via the Integrated Stress Response (ISR)R56AG075204 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HAYNES, COLE M · 2022 to 2022
$335k
NIA NIH HHS R37 AG047182NIA NIH HHS R56 AG075204
6 · The paper itself

Abstract

We review the findings that establish that perturbations of various aspects of mitochondrial function, including oxidative phosphorylation, can promote lifespan extension, with different types of perturbations acting sometimes independently and additively on extending lifespan. We also review the great variety of processes and mechanisms that together form the mitochondrial unfolded protein response. We then explore the relationships between different types of mitochondrial dysfunction-dependent lifespan extension and the mitochondrial unfolded protein response. We conclude that, although several ways that induce extended lifespan through mitochondrial dysfunction require a functional mitochondrial unfolded protein response, there is no clear indication that activation of the mitochondrial unfolded protein response is sufficient to extend lifespan, despite the fact that the mitochondrial unfolded protein response impacts almost every aspect of mitochondrial function. In fact, in some contexts, mitochondrial unfolded protein response activation is deleterious. To explain this pattern, we hypothesize that, although triggered by mitochondrial dysfunction, the lifespan extension observed might not be the result of a change in mitochondrial function.

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsAgingAnimalsLongevityMitochondriaUnfolded Protein ResponseCaenorhabditis elegans ProteinsagingmitochondriaUPRmtWormBook

Identifiers

PMID36342845
PMCPMC9713405
OpenAlexW4308371388

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.