ArticleCritical care (London, England)2022
Muscular myostatin gene expression and plasma concentrations are decreased in critically ill patients.
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.
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The trial behind it
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Muscle Dysfunction in Critical Illness: Established Mechanisms and the Potential Contribution of the NLRP3 Inflammasome.International journal of molecular sciences · 2026Review
- Muscle matters: Transforming the care of intensive care unit acquired sarcopenia and myosteatosis.World journal of clinical cases · 2025Review
- Myostatin antisense administration prevents sepsis-induced muscle atrophy and weakness in male mice.Physiological reports · 2025Article
- Myokine Secretion Dynamics and Their Role in Critically Ill Patients: A Scoping Review.Journal of clinical medicine · 2025Review
- Association of circulating muscle-derived myokines irisin and myostatin with COVID-19 severity.Frontiers in endocrinology · 2025Article
- The Significance of Selected Myokines in Predicting the Length of Rehabilitation of Patients after COVID-19 Infection.Biomedicines · 2024Article
- Utility of Plasma Myostatin as a Predictive Biomarker for Post Intensive Care Syndrome in Patients With Sepsis.Acute medicine & surgeryArticle
- Response to "Comment on 'Utility of Plasma Myostatin as a Predictive Biomarker for Post-Intensive Care Syndrome in Patients With Sepsis'".Acute medicine & surgeryArticle
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
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.
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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.