Evidence map›Paper›PMID 39325426›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

miR-96-5p expression is sufficient to induce and maintain the senescent cell fate in the absence of stress.

Fernando E Santiago, Tanvi Adige, Shamsed Mahmud, Xiao Dong, Laura J Niedernhofer, Paul D Robbins

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

6 authors.

Fernando E SantiagoInstitute on the Biology of Aging and Metabolism, University of Minnesota, Minnesota, MN 55455.ORCID 0000-0001-9514-3722
Tanvi AdigeInstitute on the Biology of Aging and Metabolism, University of Minnesota, Minnesota, MN 55455.
Shamsed MahmudInstitute on the Biology of Aging and Metabolism, University of Minnesota, Minnesota, MN 55455.ORCID 0000-0001-5666-8534
Xiao DongInstitute on the Biology of Aging and Metabolism, University of Minnesota, Minnesota, MN 55455.
Laura J NiedernhoferInstitute on the Biology of Aging and Metabolism, University of Minnesota, Minnesota, MN 55455.ORCID 0000-0002-1074-1385
Paul D RobbinsInstitute on the Biology of Aging and Metabolism, University of Minnesota, Minnesota, MN 55455.

Funding

Targeting Cellular Senescence to Extend HealthspanP01AG062413 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla, Nathan K LeBrasseur · 2019 to 2026
$28.7M
Validation and characterization of the identified variants associated with human longevity in mouse modelsU19AG056278 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI NIR J BARZILAI, Paul D. Robbins · 2017 to 2026
$24.5M
Midwest Murine-Tissue Mapping Center (MM-TMC)U54AG079754 · NIA · UNIVERSITY OF MINNESOTA · PI GR Scott Budinger, Sundeep Khosla · 2022 to 2026
$11.5M
Minnesota Tissue Mapping Center for Senescent CellsU54AG076041 · NIA · UNIVERSITY OF MINNESOTA · PI Constantin F. Aliferis, LAURA Jane NIEDERNHOFER · 2021 to 2026
$10.5M
Training Grant: Functional Proteomics of AgingT32AG029796 · NIA · UNIVERSITY OF MINNESOTA · PI EDGAR A ARRIAGA, Douglas G Mashek · 2008 to 2026
$6.6M
Defining the interactions of senescent immune cells and skeletal cellsR01AG076515 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla, David G Monroe · 2022 to 2026
$2.4M
HHS | NIH | National Institute on Aging (NIA) P01 AG062412NIA NIH HHS P01 AG062413NIA NIH HHS R01 AG076515NIA NIH HHS T32 AG029796NIA NIH HHS U19 AG056278NIA NIH HHS U54 AG076041NIA NIH HHS U54 AG079754
6 · The paper itself

Abstract

Senescence is a cell fate driven by different types of stress that results in exit from the cell cycle and expression of an inflammatory senescence-associated secretory phenotype (SASP). Here, we demonstrate that stable overexpression of miR-96-5p was sufficient to induce cellular senescence in the absence of genotoxic stress, inducing expression of certain markers of early senescence including SASP factors while repressing markers of deep senescence including LINE-1 and type 1 interferons. Stable miR-96-5p overexpression led to genome-wide changes in heterochromatin followed by epigenetic activation of p16

Indexed as

Cellular SenescenceDNA DamageMicroRNAsAnimalsCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsEndonucleasesEpigenesis, GeneticGene Expression RegulationHeterochromatinHistone DemethylasesHumansMiceRepressor ProteinsSenescence-Associated Secretory PhenotypeCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsEndonucleasesErcc1 protein, mouseHeterochromatinHistone DemethylasesMicroRNAsMIRN96 microRNA, humanMirn96 microRNA, mouseRepressor ProteinsagingepigeneticsmiRNAsenescenceSIN3B

Identifiers

PMID39325426
PMCPMC11459134

What OpenQuestion holds

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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.