Evidence map›Paper›PMID 31795499›Full record

ReviewCells2019

Amitosenescence and Pseudomitosenescence: Putative New Players in the Aging Process.

Diane Wengerodt, Christian Schmeer, Otto W Witte, Alexandra Kretz

Abstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Lamin B1 as a key modulator of the developing and aging brain.Frontiers in cellular neuroscience · 2023
    Review
  6. Article
  7. DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Frontiers in cellular and infection microbiology · 2021
    Article
  14. Cellular Senescence in Brain Aging.Frontiers in aging neuroscience · 2021
    Review
  15. 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

4 authors.

Diane WengerodtHans-Berger Department of Neurology, Jena University Hospital, 07747 Jena, Thuringia, Germany.
Christian SchmeerHans-Berger Department of Neurology, Jena University Hospital, 07747 Jena, Thuringia, Germany.
Otto W WitteHans-Berger Department of Neurology, Jena University Hospital, 07747 Jena, Thuringia, Germany.
Alexandra KretzHans-Berger Department of Neurology, Jena University Hospital, 07747 Jena, Thuringia, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Replicative senescence has initially been defined as a stress reaction of replication-competent cultured cells in vitro, resulting in an ultimate cell cycle arrest at preserved growth and viability. Classically, it has been linked to critical telomere curtailment following repetitive cell divisions, and later described as a response to oncogenes and other stressors. Currently, there are compelling new directions indicating that a comparable state of cellular senescence might be adopted also by postmitotic cell entities, including terminally differentiated neurons. However, the cellular upstream inducers and molecular downstream cues mediating a senescence-like state in neurons (amitosenescence) are ill-defined. Here, we address the phenomenon of abortive atypical cell cycle activity in light of amitosenescence, and discuss why such replicative reprogramming might provide a yet unconsidered source to explain senescence in maturated neurons. We also hypothesize the existence of a G

Indexed as

AgingCell CycleCells, CulturedCellular SenescenceHumansMitochondriaNeuronscell cyclecellular senescenceDDRGAlertpostmitotic neuronsreplicative reprogramming

Identifiers

PMID31795499
PMCPMC6952980

What OpenQuestion holds

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LicenceCC BY
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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.