Evidence map›Paper›PMID 28607003›Full record

ArticleThe EMBO journal2017

p21 maintains senescent cell viability under persistent DNA damage response by restraining JNK and caspase signaling.

Reut Yosef, Noam Pilpel, Nurit Papismadov, Hilah Gal, Yossi Ovadya, Ezra Vadai, Stav Miller, Ziv Porat, Shifra Ben-Dor, Valery Krizhanovsky

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers.

0numbers the graph read from it
0cells of the map it votes in
182citing papers in PubMed
9.3field-weighted citation impact, top 2% 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

182 citing papers in PubMed, 273 citations in OpenAlex.

  1. Article
  2. PP4 deficiency drives airway epithelial senescence via the PERK-eIF2α-ATF4-p21 axis in severe asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Transcriptional regulation in cardiovascular aging.Frontiers in cardiovascular medicine · 2026
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

122 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

10 authors at 1 institution in 1 country.

Reut YosefDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
Noam PilpelDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
Nurit PapismadovDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
Hilah GalDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
Yossi OvadyaDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
Ezra VadaiDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
Stav MillerDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
Ziv PoratLife Sciences Core Facilities, The Weizmann Institute of Science, Rehovot, Israel.
Shifra Ben-DorLife Sciences Core Facilities, The Weizmann Institute of Science, Rehovot, Israel.ORCID 0000-0001-9604-1939
Valery KrizhanovskyDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel valery.krizhanovsky@weizmann.ac.il.ORCID 0000-0002-3977-5482
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is a permanent state of cell cycle arrest that protects the organism from tumorigenesis and regulates tissue integrity upon damage and during tissue remodeling. However, accumulation of senescent cells in tissues during aging contributes to age-related pathologies. A deeper understanding of the mechanisms regulating the viability of senescent cells is therefore required. Here, we show that the CDK inhibitor p21 (CDKN1A) maintains the viability of DNA damage-induced senescent cells. Upon p21 knockdown, senescent cells acquired multiple DNA lesions that activated ataxia telangiectasia mutated (ATM) and nuclear factor (NF)-κB kinase, leading to decreased cell survival. NF-κB activation induced TNF-α secretion and JNK activation to mediate death of senescent cells in a caspase- and JNK-dependent manner. Notably, p21 knockout in mice eliminated liver senescent stellate cells and alleviated liver fibrosis and collagen production. These findings define a novel pathway that regulates senescent cell viability and fibrosis.

Indexed as

DNA DamageGene Expression RegulationMAP Kinase Signaling SystemAnimalsCaspasesCell LineCell SurvivalCyclin-Dependent Kinase Inhibitor p21HumansMiceCaspasesCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21apoptosiscellular senescenceDNA damage responseJNKp21(CDKN1A)

Identifiers

PMID28607003
PMCPMC5538795
OpenAlexW2624008928

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.