Evidence map›Paper›PMID 32264951›Full record

ArticleGenome biology2020

A multidimensional systems biology analysis of cellular senescence in aging and disease.

Roberto A Avelar, Javier Gómez Ortega, Robi Tacutu, Eleanor J Tyler, Dominic Bennett, Paolo Binetti, Arie Budovsky, Kasit Chatsirisupachai, Emily Johnson, Alex Murray and 6 more

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 269 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
269citing papers in PubMed, 2 pooled it
23.7field-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

269 citing papers in PubMed, 2 syntheses or guidelines pooled it, 389 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. AcutebioRxiv : the preprint server for biology · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Infection and immunity · 2026
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

209 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 5 countries.

Roberto A AvelarIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Javier Gómez OrtegaIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Robi TacutuIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Eleanor J TylerCentre for Cell Biology and Cutaneous Research, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, E1 2AT, UK.
Dominic BennettIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Paolo BinettiIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Arie BudovskyResearch and Development Authority, Barzilai Medical Center, Ashkelon, Israel.
Kasit ChatsirisupachaiIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Emily JohnsonIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Alex MurrayIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Samuel ShieldsIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Daniela Tejada-MartinezIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Daniel ThorntonIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Vadim E FraifeldThe Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Center for Multidisciplinary Research on Aging, Ben-Gurion University of the Negev, 8410501, Beer Sheva, Israel.
Cleo L BishopCentre for Cell Biology and Cutaneous Research, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, E1 2AT, UK. c.l.bishop@qmul.ac.uk.
João Pedro de MagalhãesIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK. jp@senescence.info.
Genomics (United Kingdom) · GBUniversity of Liverpool · GBQueen Mary University of London · GBAustral University of Chile · CLBarzilai Medical Center · ILBen-Gurion University of the Negev · ILMonash University · AU

Funding

Biotechnology and Biological Sciences Research Council BB/P002579/1Biotechnology and Biological Sciences Research Council BB/R014949/1Wellcome TrustWellcome Trust 104978/Z/14/ZWellcome Trust 208375/Z/17/Z
6 · The paper itself

Abstract

backgroundCellular senescence, a permanent state of replicative arrest in otherwise proliferating cells, is a hallmark of aging and has been linked to aging-related diseases. Many genes play a role in cellular senescence, yet a comprehensive understanding of its pathways is still lacking.

resultsWe develop CellAge (http://genomics.senescence.info/cells), a manually curated database of 279 human genes driving cellular senescence, and perform various integrative analyses. Genes inducing cellular senescence tend to be overexpressed with age in human tissues and are significantly overrepresented in anti-longevity and tumor-suppressor genes, while genes inhibiting cellular senescence overlap with pro-longevity and oncogenes. Furthermore, cellular senescence genes are strongly conserved in mammals but not in invertebrates. We also build cellular senescence protein-protein interaction and co-expression networks. Clusters in the networks are enriched for cell cycle and immunological processes. Network topological parameters also reveal novel potential cellular senescence regulators. Using siRNAs, we observe that all 26 candidates tested induce at least one marker of senescence with 13 genes (C9orf40, CDC25A, CDCA4, CKAP2, GTF3C4, HAUS4, IMMT, MCM7, MTHFD2, MYBL2, NEK2, NIPA2, and TCEB3) decreasing cell number, activating p16/p21, and undergoing morphological changes that resemble cellular senescence.

conclusionsOverall, our work provides a benchmark resource for researchers to study cellular senescence, and our systems biology analyses reveal new insights and gene regulators of cellular senescence.

Indexed as

Databases, GeneticAgingAnimalsCellular SenescenceDiseaseEvolution, MolecularGene ExpressionGenes, NeoplasmHumansLongevityOligonucleotide Array Sequence AnalysisOrgan SpecificityProtein Interaction MappingRNA-SeqSystems BiologyBiogerontologyCancerGeneticsLongevityTranscriptome

Identifiers

PMID32264951
PMCPMC7333371
OpenAlexW3014402470

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.