Evidence map›Paper›PMID 31251810›Full record

ArticleNucleic acids research2019

Transcriptome signature of cellular senescence.

Gabriel Casella, Rachel Munk, Kyoung Mi Kim, Yulan Piao, Supriyo De, Kotb Abdelmohsen, Myriam Gorospe

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 219 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
219citing papers in PubMed, 1 pooled it
18.4field-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

219 citing papers in PubMed, 1 synthesis or guideline pooled it, 353 citations in OpenAlex.

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159 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Gabriel CasellaLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland 21224, USA.
Rachel MunkLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland 21224, USA.
Kyoung Mi KimLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland 21224, USA.
Yulan PiaoLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland 21224, USA.
Supriyo DeLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland 21224, USA.
Kotb AbdelmohsenLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland 21224, USA.
Myriam GorospeLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland 21224, USA.
National Institutes of Health · US

Funding

Post-transcriptional Regulation Of Proliferative and Stress Response GenesZIAAG000511 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$25.4M
Influence of Post-transcriptional Gene Regulation on Cell Senescence and AgingZIAAG000393 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$24.1M
6 · The paper itself

Abstract

Cellular senescence, an integral component of aging and cancer, arises in response to diverse triggers, including telomere attrition, macromolecular damage and signaling from activated oncogenes. At present, senescent cells are identified by the combined presence of multiple traits, such as senescence-associated protein expression and secretion, DNA damage and β-galactosidase activity; unfortunately, these traits are neither exclusively nor universally present in senescent cells. To identify robust shared markers of senescence, we have performed RNA-sequencing analysis across eight diverse models of senescence triggered in human diploid fibroblasts (WI-38, IMR-90) and endothelial cells (HUVEC, HAEC) by replicative exhaustion, exposure to ionizing radiation or doxorubicin, and expression of the oncogene HRASG12V. The intersection of the altered transcriptomes revealed 50 RNAs consistently elevated and 18 RNAs consistently reduced across all senescence models, including many protein-coding mRNAs and some non-coding RNAs. We propose that these shared transcriptome profiles will enable the identification of senescent cells in vivo, the investigation of their roles in aging and malignancy and the development of strategies to target senescent cells therapeutically.

Indexed as

TranscriptomeAgingAntibiotics, AntineoplasticCell LineCells, CulturedCellular SenescenceDoxorubicinEndothelial CellsFibroblastsHumansNeoplasmsRadiation, IonizingRNA, MessengerSequence Analysis, RNAAntibiotics, AntineoplasticDoxorubicinRNA, Messenger

Identifiers

PMID31251810
PMCPMC6698740
OpenAlexW2954376097

What OpenQuestion holds

Textmetadata
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.