Evidence map›Paper›PMID 24897381›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Dexamethasone-induced autophagy mediates muscle atrophy through mitochondrial clearance.

Rodrigo Troncoso, Felipe Paredes, Valentina Parra, Damián Gatica, César Vásquez-Trincado, Clara Quiroga, Roberto Bravo-Sagua, Camila López-Crisosto, Andrea E Rodriguez, Alejandra P Oyarzún and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

66 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
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  13. The Impact ofInternational journal of molecular sciences · 2024
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6 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

12 authors at 3 institutions in 3 countries.

Rodrigo TroncosoAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile.
Felipe ParedesAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile.
Valentina ParraAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile; Department of Internal Medicine (Cardiology Division); University of Texas Southwestern Medical Center; Dallas, TX USA.
Damián GaticaAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile.
César Vásquez-TrincadoAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile.
Clara QuirogaAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile.
Roberto Bravo-SaguaAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile.
Camila López-CrisostoAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile.
Andrea E RodriguezAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile.
Alejandra P OyarzúnAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile.
Guido KroemerEquipe 11 labellisée pas la Ligue Nationale contre le Cancer; INSERM; Centre de Recherche des Cordeliers; Paris, France; Metabolomics and Cell Biology Platforms; Institut Gustave Roussy; Villejuif, France; Pôle de Biologie; Hôpital Européen Georges Pompidou; AP-HP; Paris, France; Université Paris Descartes; Paris Sorbonne Cité; Paris, France.
Sergio LavanderoAdvanced Center for Chronic Disease (ACCDiS); University of Chile; Santiago, Chile; Center for Molecular Studies of the Cell; Faculty of Chemical & Pharmaceutical Sciences & Faculty of Medicine; University of Chile; Santiago, Chile; Department of Internal Medicine (Cardiology Division); University of Texas Southwestern Medical Center; Dallas, TX USA.
University of Chile · CLAdvanced Center for Chronic Diseases · CLAssistance Publique – Hôpitaux de Paris · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoids, such as dexamethasone, enhance protein breakdown via ubiquitin-proteasome system. However, the role of autophagy in organelle and protein turnover in the glucocorticoid-dependent atrophy program remains unknown. Here, we show that dexamethasone stimulates an early activation of autophagy in L6 myotubes depending on protein kinase, AMPK, and glucocorticoid receptor activity. Dexamethasone increases expression of several autophagy genes, including ATG5, LC3, BECN1, and SQSTM1 and triggers AMPK-dependent mitochondrial fragmentation associated with increased DNM1L protein levels. This process is required for mitophagy induced by dexamethasone. Inhibition of mitochondrial fragmentation by Mdivi-1 results in disrupted dexamethasone-induced autophagy/mitophagy. Furthermore, Mdivi-1 increases the expression of genes associated with the atrophy program, suggesting that mitophagy may serve as part of the quality control process in dexamethasone-treated L6 myotubes. Collectively, these data suggest a novel role for dexamethasone-induced autophagy/mitophagy in the regulation of the muscle atrophy program.

Indexed as

AMP-Activated Protein KinasesAnimalsApoptosis Regulatory ProteinsAutophagyAutophagy-Related Protein 5Beclin-1Cell LineDexamethasoneDose-Response Relationship, DrugDynaminsGlucocorticoidsHeat-Shock ProteinsMicrotubule-Associated ProteinsMitochondria, MuscleMitophagyMuscle Fibers, Skeletal3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneAMP-Activated Protein KinasesAnxa3 protein, ratApoptosis Regulatory ProteinsAtg5 protein, ratAutophagy-Related Protein 5Beclin-1Becn1 protein, ratDexamethasoneDnm1l protein, ratDynaminsGlucocorticoidsHeat-Shock ProteinsMicrotubule-Associated ProteinsProteinsQuinazolinonesReceptors, GlucocorticoidSequestosome-1 ProteinSqstm1 protein, ratautophagydexamethasoneglucocorticoidmitophagymuscle atrophy

Identifiers

PMID24897381
PMCPMC4111682
OpenAlexW2050612356

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.