Evidence map›Paper›PMID 31553904›Full record

ArticleCell reports2019

SILAC Analysis Reveals Increased Secretion of Hemostasis-Related Factors by Senescent Cells.

Christopher D Wiley, Su Liu, Chandani Limbad, Anna M Zawadzka, Jennifer Beck, Marco Demaria, Robert Artwood, Fatouma Alimirah, Jose-Alberto Lopez-Dominguez, Chisaka Kuehnemann and 10 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
9.9field-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

88 citing papers in PubMed, 129 citations in OpenAlex.

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28 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

20 authors at 6 institutions in 2 countries.

Christopher D WileyBuck Institute for Research on Aging, Novato, CA 94945, USA.
Su LiuBuck Institute for Research on Aging, Novato, CA 94945, USA.
Chandani LimbadBuck Institute for Research on Aging, Novato, CA 94945, USA.
Anna M ZawadzkaBuck Institute for Research on Aging, Novato, CA 94945, USA.
Jennifer BeckBuck Institute for Research on Aging, Novato, CA 94945, USA.
Marco DemariaEuropean Institute for the Biology of Aging, University of Groningen, Groningen, the Netherlands.
Robert ArtwoodBuck Institute for Research on Aging, Novato, CA 94945, USA.
Fatouma AlimirahBuck Institute for Research on Aging, Novato, CA 94945, USA.
Jose-Alberto Lopez-DominguezBuck Institute for Research on Aging, Novato, CA 94945, USA.
Chisaka KuehnemannBuck Institute for Research on Aging, Novato, CA 94945, USA.
Steven R DanielsonBuck Institute for Research on Aging, Novato, CA 94945, USA.
Natan BasistyBuck Institute for Research on Aging, Novato, CA 94945, USA.
Herbert G KaslerBuck Institute for Research on Aging, Novato, CA 94945, USA.
Tal Ronnen OronBuck Institute for Research on Aging, Novato, CA 94945, USA.
Pierre-Yves DesprezBuck Institute for Research on Aging, Novato, CA 94945, USA; California Pacific Medical Center, Research Institute, San Francisco, CA 94107, USA.
Sean D MooneyDepartment of Biomedical Informatics & Medical Education, University of Washington, Seattle, WA 98195, USA.
Bradford W GibsonDiscovery Attribute Sciences, Amgen Inc., South San Francisco, CA 94080, USA.
Birgit SchillingBuck Institute for Research on Aging, Novato, CA 94945, USA.
Judith CampisiBuck Institute for Research on Aging, Novato, CA 94945, USA; Biosciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA. Electronic address: jcampisi@buckinstitute.org.
Pankaj KapahiBuck Institute for Research on Aging, Novato, CA 94945, USA. Electronic address: pkapahi@buckinstitute.org.
Buck Institute for Research on Aging · USAmgen (United States) · USCalifornia Pacific Medical Center · USLawrence Berkeley National Laboratory · USUniversity of Groningen · NLUniversity of Washington · US

Funding

Systems Biology and Bioinformatics CoreP01AG041122 · NIA · MAYO CLINIC ROCHESTER · PI CAMPISI, JUDITH · 2012 to 2016
$9.8M
CELLULAR SENESCENCE AND CONTROL OF GENE EXPRESSIONR37AG009909 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI CAMPISI, JUDITH · 1995 to 2015
$7.6M
Cellular Senescence, astrocytes and Alzheimer's diseaseR01AG051729 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI CAMPISI, JUDITH · 2016 to 2020
$2.7M
Molecular Mechanisms of Lifespan Extension by Dietary Restriction in DrosophilaR01AG038688 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI KAPAHI, PANKAJ · 2011 to 2015
$2.3M
Molecular Mechanisms of Lifespan Extension by Dietary Restriction in DrosophilaR56AG038688 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI KAPAHI, PANKAJ · 2017 to 2017
$612k
TripleTOF 5600 High Resolution Mass SpectrometerS10OD016281 · OD · BUCK INSTITUTE FOR RESEARCH ON AGING · PI GIBSON, BRADFORD WAYNE · 2013 to 2013
$597k
Cellular senescence and control of gene expressionR56AG009909 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI CAMPISI, JUDITH · 2017 to 2017
$592k
Role of mTOR Pathway in Cellular SenescenceF32AG043252 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI LIU, SU · 2012 to 2014
$163k
NIA NIH HHS F32 AG043252NIA NIH HHS P01 AG041122NIA NIH HHS R01 AG038688NIA NIH HHS R01 AG051729NIA NIH HHS R37 AG009909NIA NIH HHS R56 AG009909NIA NIH HHS R56 AG038688NIH HHS S10 OD016281
6 · The paper itself

Abstract

Cellular senescence irreversibly arrests cell proliferation, accompanied by a multi-component senescence-associated secretory phenotype (SASP) that participates in several age-related diseases. Using stable isotope labeling with amino acids (SILACs) and cultured cells, we identify 343 SASP proteins that senescent human fibroblasts secrete at 2-fold or higher levels compared with quiescent cell counterparts. Bioinformatic analysis reveals that 44 of these proteins participate in hemostasis, a process not previously linked with cellular senescence. We validated the expression of some of these SASP factors in cultured cells and in vivo. Mice treated with the chemotherapeutic agent doxorubicin, which induces widespread cellular senescence in vivo, show increased blood clotting. Conversely, selective removal of senescent cells using transgenic p16-3MR mice showed that clearing senescent cells attenuates the increased clotting caused by doxorubicin. Our study provides an in-depth, unbiased analysis of the SASP and unveils a function for cellular senescence in hemostasis.

Indexed as

Cellular SenescenceHemostasisHumansagingcellular senescencechemotherapyclottingcoagulationhomeostasisproteomicsSASPsecretionthrombosis

Identifiers

PMID31553904
PMCPMC6907691
OpenAlexW2977045310

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.