ArticleJournal of bone metabolism2020
Myostatin Inhibitors: Panacea or Predicament for Musculoskeletal Disorders?
Article in Journal of bone metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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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.
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.
Who cites it
55 citing papers in PubMed, 77 citations in OpenAlex.
- Trial
- Exerkines in precision management of metabolic diseases.Chinese medical journal · 2026Review
- ITCH-Mediated Ubiquitination and Degradation of THBS1: A Key Mechanism for Enhancing Mitochondrial Biogenesis and Alleviating Mouse Skeletal Muscle Atrophy.Acta physiologica (Oxford, England) · 2026Article
- Sarcopenia and Skeletal Muscle Dysfunction in Liver Cirrhosis: Clinical Perspectives of Myostatin Inhibition.Biomedicines · 2026Review
- Strategies to mitigate muscle mass loss in individuals with spinal cord injury.The journal of spinal cord medicine · 2026Review
- Loss of LCN2 Function Ameliorates Glucocorticoid-Induced Muscle Atrophy via Remodeling the Extracellular Matrix.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Swimming exercise training (SET) and MitoQ supplementation can mitigate the atrophy and inflammation process in skeletal muscles of male Wistar rats with spinal cord injury (SCI): NF-κB/MuRF-1/proteasome pathway.Biochemistry and biophysics reports · 2026Article
- Exerkine dysregulation links visceral adiposity to skeletal muscle impairment in end-stage heart failure with reduced ejection fraction: proteomic evidence for a cardio-adipose-muscle axis.Cardiovascular diabetology · 2026Article
- Sarcopenia in Kidney Transplantation: Bridging Pathophysiology to Patient-Centered Care.Nutrients · 2026Review
- Obesity and bone health: reconciling the density-fragility paradox.Frontiers in endocrinology · 2026Review
- The sarcopenia-pain connection: why mechanisms matter for patient care?Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- Myostatin inhibitors in sarcopenia treatment: A comprehensive review of mechanisms, efficacy and future directions.Molecular biology reports · 2025Review
- Dynamic Anchoring of Peptides to the Extracellular Matrix Enabled by Boronic Acid.Chembiochem : a European journal of chemical biology · 2025Article
- Potent and durable gene modulation in heart and muscle with chemically defined lipophilic siRNAs.Nucleic acids research · 2025Article
- The functions of MicroRNAs in myogenesis and their effects in beef cattle meat quality: a review.Molecular biology reports · 2025Review
- Emerging Role of Myostatin Inhibitors in the Management of Glucagon-Like Peptide-1-Associated Sarcopenia and Metabolic Disorders.Journal of bone metabolism · 2025Article
- Myostatin Function during In Vitro Myogenesis: Considerations for Knockout-Based Mechanistic Analysis.Journal of bone metabolism · 2025Article
- Sheer drop ahead: reviewing sarcopenia outcomes in elderly patients undergoing bariatric surgery.Reviews in endocrine & metabolic disorders · 2025Review
- Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025Review
- Glucocorticoid-Mediated Skeletal Muscle Atrophy: Molecular Mechanisms and Potential Therapeutic Targets.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myostatin, also known as growth differentiation factor 8 (GDF8), is a transforming growth factor-β (TGF-β) family member that functions to limit skeletal muscle growth. Accordingly, loss-of-function mutations in myostatin result in a dramatic increase in muscle mass in humans and various animals, while its overexpression leads to severe muscle atrophy. Myostatin also exerts a significant effect on bone metabolism, as demonstrated by enhanced bone mineral density and bone regeneration in myostatin null mice. The identification of myostatin as a negative regulator of muscle and bone mass has sparked an enormous interest in developing myostatin inhibitors as therapeutic agents for treating a variety of clinical conditions associated with musculoskeletal disorders. As a result, various myostatin-targeting strategies involving antibodies, myostatin propeptides, soluble receptors, and endogenous antagonists have been generated, and many of them have progressed to clinical trials. Importantly, most myostatin inhibitors also repress the activities of other closely related TGF-β family members including GDF11, activins, and bone morphogenetic proteins (BMPs), increasing the potential for unwanted side effects, such as vascular side effects through inhibition of BMP 9/10 and bone weakness induced by follistatin through antagonizing several TGF-β family members. Therefore, a careful distinction between targets that may enhance the efficacy of an agent and those that may cause adverse effects is required with the improvement of the target specificity. In this review, we discuss the current understanding of the endogenous function of myostatin, and provide an overview of clinical trial outcomes from different myostatin inhibitors.
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Registered trials
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.