Evidence map›Paper›PMID 38385946›Full record

ArticleThe Journal of experimental medicine2024

Cellular senescence: Neither irreversible nor reversible.

Maurice Reimann, Soyoung Lee, Clemens A Schmitt

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
29.1field-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

76 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
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  8. p16 Beyond Senescence: Cancer Biology Lessons Applied to Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  9. Article
  10. Review
  11. Review
  12. Pre-Encoded IFN-I Sensitivity Exacerbates Memory T Cell Senescence in Solid Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  13. Article
  14. Review
  15. The Aging Kidney and Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2026
    Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

16 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 2 institutions in 2 countries.

Maurice ReimannMedical Department of Hematology, Oncology and Tumor Immunology, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, and Molekulares Krebsforschungszentrum-MKFZ, Campus Virchow Klinikum, Charité-Universitätsmedizin, Berlin, Germany.ORCID 0000-0002-7876-0128
Soyoung LeeMedical Department of Hematology, Oncology and Tumor Immunology, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, and Molekulares Krebsforschungszentrum-MKFZ, Campus Virchow Klinikum, Charité-Universitätsmedizin, Berlin, Germany.ORCID 0000-0002-4614-2931
Clemens A SchmittMedical Department of Hematology, Oncology and Tumor Immunology, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, and Molekulares Krebsforschungszentrum-MKFZ, Campus Virchow Klinikum, Charité-Universitätsmedizin, Berlin, Germany.ORCID 0000-0002-4731-2226
Johannes Kepler University of Linz · ATCharité - Universitätsmedizin Berlin · DE

Funding

Deutsche Forschungsgemeinschaft GO 2688/1-1 SCHM 1633/11-1Deutsche Krebshilfe 7011377629Förderverein Hämatologie und Internistische Onkologie (Tyle Private Foundation)German BMBF e:Med 031L0189A
6 · The paper itself

Abstract

Cellular senescence is a critical stress response program implicated in embryonic development, wound healing, aging, and immunity, and it backs up apoptosis as an ultimate cell-cycle exit mechanism. In analogy to replicative exhaustion of telomere-eroded cells, premature types of senescence-referring to oncogene-, therapy-, or virus-induced senescence-are widely considered irreversible growth arrest states as well. We discuss here that entry into full-featured senescence is not necessarily a permanent endpoint, but dependent on essential maintenance components, potentially transient. Unlike a binary state switch, we view senescence with its extensive epigenomic reorganization, profound cytomorphological remodeling, and distinctive metabolic rewiring rather as a journey toward a full-featured arrest condition of variable strength and depth. Senescence-underlying maintenance-essential molecular mechanisms may allow cell-cycle reentry if not continuously provided. Importantly, senescent cells that resumed proliferation fundamentally differ from those that never entered senescence, and hence would not reflect a reversion but a dynamic progression to a post-senescent state that comes with distinct functional and clinically relevant ramifications.

Indexed as

AgingCellular SenescenceApoptosisCell CycleCell DivisionFemaleHumansPregnancy

Identifiers

PMID38385946
PMCPMC10883852
OpenAlexW4392058541

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.