Evidence map›Paper›PMID 29989354›Full record

ArticleJournal of cachexia, sarcopenia and muscle2018

Increased Serpina3n release into circulation during glucocorticoid-mediated muscle atrophy.

Marine Gueugneau, Donatienne d'Hose, Caroline Barbé, Marie de Barsy, Pascale Lause, Dominique Maiter, Laure B Bindels, Nathalie M Delzenne, Laurent Schaeffer, Yann-Gaël Gangloff and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 72 citations in OpenAlex.

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  15. Skeletal muscle omics signatures in cancer cachexia: perspectives and opportunities.Journal of the National Cancer Institute. Monographs · 2023
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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

14 authors at 4 institutions in 2 countries.

Marine GueugneauPole of Endocrinology, Diabetes and Nutrition, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.ORCID 0000-0001-8871-7345
Donatienne d'HosePole of Endocrinology, Diabetes and Nutrition, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Caroline BarbéPole of Endocrinology, Diabetes and Nutrition, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Marie de BarsyPole of Endocrinology, Diabetes and Nutrition, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Pascale LausePole of Endocrinology, Diabetes and Nutrition, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Dominique MaiterPole of Endocrinology, Diabetes and Nutrition, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Laure B BindelsMetabolism and Nutrition Research Group, Louvain Drug Research Institute (LDRI), Université catholique de Louvain, Brussels, Belgium.
Nathalie M DelzenneMetabolism and Nutrition Research Group, Louvain Drug Research Institute (LDRI), Université catholique de Louvain, Brussels, Belgium.
Laurent SchaefferINMG, CNRS, UMR 5310, INSERM U1217, LBMC, Ecole Normale Supérieure de Lyon, Lyon, France.
Yann-Gaël GangloffINMG, CNRS, UMR 5310, INSERM U1217, LBMC, Ecole Normale Supérieure de Lyon, Lyon, France.
Christophe ChambonINRA, Plateforme d'Exploration du Métabolisme Composante Protéomique, Saint Genès Champanelle, France.
Cécile Coudy-GandilhonINRA, UMR1019, Université Clermont Auvergne, UNH, Unité de Nutrition Humaine, CRNH Auvergne, Clermont-Ferrand, France.
Daniel BéchetINRA, UMR1019, Université Clermont Auvergne, UNH, Unité de Nutrition Humaine, CRNH Auvergne, Clermont-Ferrand, France.
Jean-Paul ThissenPole of Endocrinology, Diabetes and Nutrition, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
International Diabetes Federation · BEUniversité Clermont Auvergne · FRSolvay (Belgium) · BEUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlucocorticoids (GC) play a major role in muscle atrophy. As skeletal muscle is a secretory organ, characterization of the muscle secretome elicited by muscle atrophy should allow to better understand the cellular mechanisms and to identify circulating biomarkers of this condition. Our project aimed to identify the changes in the muscle secretome associated with GC-induced muscle atrophy and susceptible to translate into circulation.

methodsWe have identified the GC-induced changes in the secretome of C

resultsThis approach led us to identify Serpina3n as one of the most markedly secreted protein in response to GC. Our original in vitro results were confirmed in vivo by an increased expression of Serpina3n in skeletal muscle (3.9-fold; P < 0.01) and in the serum (two-fold; P < 0.01) of mice treated with GC. We also observed increased levels of the human orthologue Serpina3 in the serum of Cushing's syndrome patients compared with healthy controls matched for age and sex (n = 9/group, 2.5-fold; P < 0.01). An increase of Serpina3n was also demonstrated in muscle atrophy models mediated by GC such as cancer cachexia (four-fold; P < 0.01), sepsis (12.5-fold; P < 0.001), or diabetes (two-fold; P < 0.01). In contrast, levels of Serpina3n both in skeletal muscle and in the circulation were reduced in several models of muscle hypertrophy induced by myostatin inhibition (P < 0.01). Furthermore, a cluster of data suggests that the regulation of muscle Serpina3n involves mTOR, an essential determinant of the muscle cell size.

conclusionsTaken together, these data suggest that Serpina3n may represent a circulating biomarker of muscle atrophy associated to GC and, broadly, a reflection of dynamic changes in muscle mass.

Indexed as

AnimalsCase-Control StudiesCell LineCells, CulturedCell SurvivalChromatography, LiquidCushing SyndromeDexamethasoneDisease Models, AnimalGene ExpressionGlucocorticoidsHumansMaleMiceMuscular AtrophyMyoblastsDexamethasoneGlucocorticoidsProteomeSERPINA3 protein, humanSerpinsBiomarkerGlucocorticoidsMuscle atrophySerpina3n

Identifiers

PMID29989354
PMCPMC6204594
OpenAlexW2865323408

What OpenQuestion holds

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LicenceCC BY-NC
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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.