Evidence map›Paper›PMID 32369550›Full record

ReviewBiochemical Society transactions2020

Functional heterogeneity in senescence.

Kristina Kirschner, Nattaphong Rattanavirotkul, Megan F Quince, Tamir Chandra

Open access · hybridAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 88 citations in OpenAlex.

  1. Rhenium-Based β-Galactosidase Probe Allows Senescence Profiling by Mass Cytometry.Angewandte Chemie (International ed. in English) · 2026
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2 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

4 authors at 3 institutions in 2 countries.

Kristina KirschnerInstitute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, U.K.
Nattaphong RattanavirotkulChakri Naruebodindra Medical Institute, Mahidol University, Samut Prakan 10540, Thailand.
Megan F QuinceInstitute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, U.K.
Tamir ChandraMRC Human Genetics Unit, University of Edinburgh, Edinburgh EH4 2XU, U.K.
University of Glasgow · GBInstitute of Genetics and Cancer · GBMahidol University · TH

Funding

Wellcome Trust 206194
6 · The paper itself

Abstract

Senescence is a tumour suppressor mechanism which is cell-intrinsically activated in the context of cellular stress. Senescence can further be propagated to neighbouring cells, a process called secondary senescence induction. Secondary senescence was initially shown as a paracrine response to the secretion of cytokines from primary senescent cells. More recently, juxtacrine Notch signalling has been implicated in mediating secondary senescence induction. Primary and secondary senescent induction results in distinct transcriptional outcomes. In addition, cell type and the stimulus in which senescence is induced can lead to variations in the phenotype of the senescence response. It is unclear whether heterogeneous senescent end-points are associated with distinct cellular function in situ, presenting functional heterogeneity. Thus, understanding senescence heterogeneity could prove to be important when devising ways of targeting senescent cells by senolytics, senostatics or senogenics. In this review, we discuss a role for functional heterogeneity in senescence in tissue- and cell-type specific manners, highlighting potential differences in senescence outcomes of primary and secondary senescence.

Indexed as

Cellular SenescenceAnimalsCytokinesDiploidyFibroblastsFibrosisHumansInsulin-Secreting CellsKidneyMicePancreasPhenotypeReceptors, NotchSignal TransductionSkinWound HealingCytokinesReceptors, NotchheterogeneityNotchsecondary senescencesenescencesenotherapy

Identifiers

PMID32369550
PMCPMC7329341
OpenAlexW3023648450

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.