Evidence map›Paper›PMID 28844647›Full record

ArticleCurrent biology : CB2017

Unmasking Transcriptional Heterogeneity in Senescent Cells.

Alejandra Hernandez-Segura, Tristan V de Jong, Simon Melov, Victor Guryev, Judith Campisi, Marco Demaria

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 588 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
588citing papers in PubMed, 1 pooled it
28.2field-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

588 citing papers in PubMed, 1 synthesis or guideline pooled it, 881 citations in OpenAlex.

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528 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

6 authors at 3 institutions in 2 countries.

Alejandra Hernandez-SeguraEuropean Research Institute for the Biology of Aging, University of Groningen, University Medical Center Groningen, Antonius Deusinglaan 1, 9713 AV Groningen, the Netherlands.
Tristan V de JongEuropean Research Institute for the Biology of Aging, University of Groningen, University Medical Center Groningen, Antonius Deusinglaan 1, 9713 AV Groningen, the Netherlands.
Simon MelovBuck Institute for Research on Aging, 8001 Redwood Boulevard, 94945 Novato CA, USA.
Victor GuryevEuropean Research Institute for the Biology of Aging, University of Groningen, University Medical Center Groningen, Antonius Deusinglaan 1, 9713 AV Groningen, the Netherlands.
Judith CampisiBuck Institute for Research on Aging, 8001 Redwood Boulevard, 94945 Novato CA, USA; Lawrence Berkeley National Laboratory, Life Sciences Division, 1 Cyclotron Road, Berkeley, CA 94720, USA.
Marco DemariaEuropean Research Institute for the Biology of Aging, University of Groningen, University Medical Center Groningen, Antonius Deusinglaan 1, 9713 AV Groningen, the Netherlands. Electronic address: m.demaria@umcg.nl.
Buck Institute for Research on Aging · USUniversity Medical Center Groningen · NLUniversity of Groningen · NL

Funding

THE IMPACT OF CELLULAR DEFENSE ON THE ROLE OF Ku80 IN GENOME MAINTENANCE AND LONGP01AG017242 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 1999 to 2023
$46.1M
NIA NIH HHS P01 AG017242
6 · The paper itself

Abstract

Cellular senescence is a state of irreversibly arrested proliferation, often induced by genotoxic stress [1]. Senescent cells participate in a variety of physiological and pathological conditions, including tumor suppression [2], embryonic development [3, 4], tissue repair [5-8], and organismal aging [9]. The senescence program is variably characterized by several non-exclusive markers, including constitutive DNA damage response (DDR) signaling, senescence-associated β-galactosidase (SA-βgal) activity, increased expression of the cyclin-dependent kinase (CDK) inhibitors p16INK4A (CDKN2A) and p21CIP1 (CDKN1A), increased secretion of many bio-active factors (the senescence-associated secretory phenotype, or SASP), and reduced expression of the nuclear lamina protein LaminB1 (LMNB1) [1]. Many senescence-associated markers result from altered transcription, but the senescent phenotype is variable, and methods for clearly identifying senescent cells are lacking [10]. Here, we characterize the heterogeneity of the senescence program using numerous whole-transcriptome datasets generated by us or publicly available. We identify transcriptome signatures associated with specific senescence-inducing stresses or senescent cell types and identify and validate genes that are commonly differentially regulated. We also show that the senescent phenotype is dynamic, changing at varying intervals after senescence induction. Identifying novel transcriptome signatures to detect any type of senescent cell or to discriminate among diverse senescence programs is an attractive strategy for determining the diverse biological roles of senescent cells and developing specific drug targets.

Indexed as

TranscriptomeAnimalsCell LineCellular SenescenceHumansRatscell-cycle arrestcellular senescenceDNA damageprimary cellsqPCRRNA-seqSASPtranscriptional signaturestumor suppressionwhole-transcriptome sequencing

Identifiers

PMID28844647
PMCPMC5788810
OpenAlexW2749511637

What OpenQuestion holds

Textmetadata
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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.