Evidence map›Paper›PMID 32300964›Full record

ReviewGeroScience2020

Regulation of senescence traits by MAPKs.

Carlos Anerillas, Kotb Abdelmohsen, Myriam Gorospe

Open access · bronzeAbstract readReview
In one paragraph

Review in GeroScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
10.0field-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

95 citing papers in PubMed, 158 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. p16 Beyond Senescence: Cancer Biology Lessons Applied to Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Parallel Selection for Longevity in Mammals and Birds.bioRxiv : the preprint server for biology · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The Implications of Alternative Splicing Regulation for Maximum Lifespan.bioRxiv : the preprint server for biology · 2025
    Article
  20. Article

35 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

3 authors at 1 institution in 1 country.

Carlos AnerillasLaboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health, 251 Bayview Blvd., Baltimore, MD, 21224, USA.ORCID 0000-0003-4424-7913
Kotb AbdelmohsenLaboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health, 251 Bayview Blvd., Baltimore, MD, 21224, USA.ORCID 0000-0001-6240-5810
Myriam GorospeLaboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health, 251 Bayview Blvd., Baltimore, MD, 21224, USA. myriam-gorospe@nih.gov.ORCID 0000-0001-5439-3434
National Institutes of Health · US

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
Influence of mRNA Turnover on the Biology of Cellular Senescence and AgingZ01AG000393 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM NONE · 2008 to 2008
$265k
Intramural NIH HHS Z01 AG000393
6 · The paper itself

Abstract

A phenotype of indefinite growth arrest acquired in response to sublethal damage, cellular senescence affects normal aging and age-related disease. Mitogen-activated protein kinases (MAPKs) are capable of sensing changes in cellular conditions, and in turn elicit adaptive responses including cell senescence. MAPKs modulate the levels and function of many proteins, including proinflammatory factors and factors in the p21/p53 and p16/RB pathways, the main senescence-regulatory axes. Through these actions, MAPKs implement key traits of senescence-growth arrest, cell survival, and the senescence-associated secretory phenotype (SASP). In this review, we summarize and discuss our current knowledge of the impact of MAPKs in senescence. In addition, given that eliminating or suppressing senescent cells can improve health span, we discuss the function and possible exploitation of MAPKs in the elimination (senolysis) or suppression (senostasis) of senescent cells.

Indexed as

Cellular SenescenceMitogen-Activated Protein KinasesSignal Transductionp38 Mitogen-Activated Protein KinasesPhenotypeMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesERKGene expression programsJNKp38SASPSenescence

Identifiers

PMID32300964
PMCPMC7205942
OpenAlexW3017101038

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.