Evidence map›Paper›PMID 29592859›Full record

ArticleEMBO reports2018

Stress granules counteract senescence by sequestration of PAI-1.

Amr Omer, Devang Patel, Xian Jin Lian, Jason Sadek, Sergio Di Marco, Arnim Pause, Myriam Gorospe, Imed Eddine Gallouzi

Abstract read
In one paragraph

Article in EMBO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
–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

44 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Shift of the insoluble content of the proteome in the aging mouse brain.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Pooled it
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  12. Connecting the Dots: Stress Granule and Cardiovascular Diseases.Journal of cardiovascular translational research · 2025
    Review
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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.

Amr OmerDepartment of Biochemistry, Rosalind and Morris Goodman Cancer Centre, McGill University, Montreal, QC, Canada.
Devang PatelDepartment of Biochemistry, Rosalind and Morris Goodman Cancer Centre, McGill University, Montreal, QC, Canada.
Xian Jin LianDepartment of Biochemistry, Rosalind and Morris Goodman Cancer Centre, McGill University, Montreal, QC, Canada.
Jason SadekDepartment of Biochemistry, Rosalind and Morris Goodman Cancer Centre, McGill University, Montreal, QC, Canada.
Sergio Di MarcoDepartment of Biochemistry, Rosalind and Morris Goodman Cancer Centre, McGill University, Montreal, QC, Canada.
Arnim PauseDepartment of Biochemistry, Rosalind and Morris Goodman Cancer Centre, McGill University, Montreal, QC, Canada.
Myriam GorospeLaboratory of Genetics and Genomics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD, USA.
Imed Eddine GallouziDepartment of Biochemistry, Rosalind and Morris Goodman Cancer Centre, McGill University, Montreal, QC, Canada imed.gallouzi@mcgill.ca igallouzi@kbku.edu.qa.ORCID 0000-0003-4758-4835

Funding

Post-transcriptional Regulation Of Proliferative and Stress Response GenesZIAAG000511 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$25.4M
Influence of Post-transcriptional Gene Regulation on Cell Senescence and AgingZIAAG000393 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$24.1M
CIHR MOP‐89798
6 · The paper itself

Abstract

Cellular senescence is a physiological response by which an organism halts the proliferation of potentially harmful and damaged cells. However, the accumulation of senescent cells over time can become deleterious leading to diseases and physiological decline. Our data reveal a novel interplay between senescence and the stress response that affects both the progression of senescence and the behavior of senescent cells. We show that constitutive exposure to stress induces the formation of stress granules (SGs) in proliferative and presenescent cells, but not in fully senescent cells. Stress granule assembly alone is sufficient to decrease the number of senescent cells without affecting the expression of bona fide senescence markers. SG-mediated inhibition of senescence is associated with the recruitment of the plasminogen activator inhibitor-1 (PAI-1), a known promoter of senescence, to these entities. PAI-1 localization to SGs increases the translocation of cyclin D1 to the nucleus, promotes RB phosphorylation, and maintains a proliferative, non-senescent state. Together, our data indicate that SGs may be targets of intervention to modulate senescence in order to impair or prevent its deleterious effects.

Indexed as

Cellular SenescenceStress, PhysiologicalCell LineCell NucleusCyclin D1Cytoplasmic GranulesHumansPhosphorylationPlasminogen Activator Inhibitor 1Cyclin D1Plasminogen Activator Inhibitor 1PAI‐1senescencestress granulesstress response

Identifiers

PMID29592859
PMCPMC5934773

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.