Evidence map›Paper›PMID 31092814›Full record

ArticleCell death & disease2019

Autophagy-induced senescence is regulated by p38α signaling.

Konstantin Slobodnyuk, Nevenka Radic, Saška Ivanova, Anna Llado, Natalia Trempolec, Antonio Zorzano, Angel R Nebreda

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 79 citations in OpenAlex.

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  19. Multiparametric identification of putative senescent cells in skeletal muscle via mass cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2024
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4 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

7 authors at 3 institutions in 1 country.

Konstantin SlobodnyukInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.
Nevenka RadicInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.
Saška IvanovaInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.
Anna LladoInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.
Natalia TrempolecInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.
Antonio ZorzanoInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain.ORCID http://orcid.org/0000-0002-1638-0306
Angel R NebredaInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028, Barcelona, Spain. angel.nebreda@irbbarcelona.org.
Institute for Research in Biomedicine · ESInstituto de Salud Carlos III · ESInstitució Catalana de Recerca i Estudis Avançats · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis and senescence are two mutually exclusive cell fate programs that can be activated by stress. The factors that instruct cells to enter into senescence or apoptosis are not fully understood, but both programs can be regulated by the stress kinase p38α. Using an inducible system that specifically activates this pathway, we show that sustained p38α activation suffices to trigger massive autophagosome formation and to enhance the basal autophagic flux. This requires the concurrent effect of increased mitochondrial reactive oxygen species production and the phosphorylation of the ULK1 kinase on Ser-555 by p38α. Moreover, we demonstrate that macroautophagy induction by p38α signaling determines that cancer cells preferentially enter senescence instead of undergoing apoptosis. In agreement with these results, we present evidence that the induction of autophagy by p38α protects cancer cells from chemotherapy-induced apoptosis by promoting senescence. Our results identify a new mechanism of p38α-regulated basal autophagy that controls the fate of cancer cells in response to stress.

Indexed as

AutophagyCellular SenescenceApoptosisAutophagy-Related Protein-1 HomologCell Line, TumorDoxorubicinHumansIntracellular Signaling Peptides and ProteinsMAP Kinase Kinase 6MitochondriaMitogen-Activated Protein Kinase 12Mitogen-Activated Protein Kinase 14PhosphorylationReactive Oxygen SpeciesRNA InterferenceRNA, Small InterferingAutophagy-Related Protein-1 HomologDoxorubicinIntracellular Signaling Peptides and ProteinsMAP2K6 protein, humanMAP Kinase Kinase 6Mitogen-Activated Protein Kinase 12Mitogen-Activated Protein Kinase 14Reactive Oxygen SpeciesRNA, Small InterferingSequestosome-1 ProteinSQSTM1 protein, humanULK1 protein, human

Identifiers

PMID31092814
PMCPMC6520338
OpenAlexW2945298403

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.