Evidence map›Paper›PMID 35922829›Full record

ArticleCritical care (London, England)2022

Muscular myostatin gene expression and plasma concentrations are decreased in critically ill patients.

Julius J Grunow, Katja Reiher, Niklas M Carbon, Lilian Jo Engelhardt, Knut Mai, Susanne Koch, Joerg C Schefold, Werner Z'Graggen, Stefan J Schaller, Jens Fielitz and 3 more

Open access · goldAbstract read
In one paragraph

Article in Critical care (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

Julius J GrunowDepartment of Anesthesiology and Operative Intensive Care Medicine (CCM/CVK), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13357, Berlin, Germany.
Katja ReiherDepartment of Anesthesiology and Operative Intensive Care Medicine (CCM/CVK), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13357, Berlin, Germany.
Niklas M CarbonDepartment of Anesthesiology and Operative Intensive Care Medicine (CCM/CVK), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13357, Berlin, Germany.
Lilian Jo EngelhardtDepartment of Anesthesiology and Operative Intensive Care Medicine (CCM/CVK), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13357, Berlin, Germany.
Knut MaiDepartment of Endocrinology and Metabolic Diseases, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Susanne KochDepartment of Anesthesiology and Operative Intensive Care Medicine (CCM/CVK), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13357, Berlin, Germany.
Joerg C SchefoldDepartment of Intensive Care Medicine, Inselspital, Bern University Hospital, University Bern, Freiburgstrasse 18, 3010, Bern, Switzerland.
Werner Z'GraggenDepartments of Neurology and Neurosurgery, Inselspital, Bern University Hospital, University Bern, Freiburgstrasse 18, 3010, Bern, Switzerland.
Stefan J SchallerDepartment of Anesthesiology and Operative Intensive Care Medicine (CCM/CVK), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13357, Berlin, Germany.
Jens FielitzCharité - Universitätsmedizin Berlin, Max Delbrück Center (MDC) for Molecular Medicine in the Helmholtz Association, Experimental and Clinical Research Center (ECRC), Lindenberger Weg 80, 13125, Berlin, Germany.
Joachim SprangerDepartment of Endocrinology and Metabolic Diseases, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Steffen Weber-CarstensDepartment of Anesthesiology and Operative Intensive Care Medicine (CCM/CVK), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13357, Berlin, Germany. steffen.weber-carstens@charite.de.ORCID 0000-0001-7405-0172
Tobias WollersheimDepartment of Anesthesiology and Operative Intensive Care Medicine (CCM/CVK), Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13357, Berlin, Germany.
Humboldt-Universität zu Berlin · DEUniversity Hospital of Bern · CHMax Delbrück Center · DE

Funding

Berlin Institute of Health Clinician ScientistBerlin Institute of Health Junior Clinician ScientistDeutsche Forschungsgemeinschaft FI 965/5-1Deutsche Forschungsgemeinschaft KFO-192Deutsches Zentrum für Herz-Kreislaufforschung 81Z5400153
6 · The paper itself

Abstract

backgroundThe objective was to investigate the role of gene expression and plasma levels of the muscular protein myostatin in intensive care unit-acquired weakness (ICUAW). This was performed to evaluate a potential clinical and/or pathophysiological rationale of therapeutic myostatin inhibition.

methodsA retrospective analysis from pooled data of two prospective studies to assess the dynamics of myostatin plasma concentrations (day 4, 8 and 14) and myostatin gene (MSTN) expression levels in skeletal muscle (day 15) was performed. Associations of myostatin to clinical and electrophysiological outcomes, muscular metabolism and muscular atrophy pathways were investigated.

resultsMSTN gene expression (median [IQR] fold change: 1.00 [0.68-1.54] vs. 0.26 [0.11-0.80]; p = 0.004) and myostatin plasma concentrations were significantly reduced in all critically ill patients when compared to healthy controls. In critically ill patients, myostatin plasma concentrations increased over time (median [IQR] fold change: day 4: 0.13 [0.08/0.21] vs. day 8: 0.23 [0.10/0.43] vs. day 14: 0.40 [0.26/0.61]; p < 0.001). Patients with ICUAW versus without ICUAW showed significantly lower MSTN gene expression levels (median [IQR] fold change: 0.17 [0.10/0.33] and 0.51 [0.20/0.86]; p = 0.047). Myostatin levels were directly correlated with muscle strength (correlation coefficient 0.339; p = 0.020) and insulin sensitivity index (correlation coefficient 0.357; p = 0.015). No association was observed between myostatin plasma concentrations as well as MSTN expression levels and levels of mobilization, electrophysiological variables, or markers of atrophy pathways.

conclusionMuscular gene expression and systemic protein levels of myostatin are downregulated during critical illness. The previously proposed therapeutic inhibition of myostatin does therefore not seem to have a pathophysiological rationale to improve muscle quality in critically ill patients.

trial registrationISRCTN77569430 -13th of February 2008 and ISRCTN19392591 17th of February 2011.

Indexed as

Critical IllnessMyostatinGene ExpressionHumansMuscle, SkeletalMuscular AtrophyProspective StudiesRetrospective StudiesMyostatinCritical illnessICUAWInsulin resistanceMuscle atrophyMyostatin

Identifiers

PMID35922829
PMCPMC9347123
OpenAlexW4289544346

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Registered trials

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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.