ArticleeLife2022
Sex-specific role of myostatin signaling in neonatal muscle growth, denervation atrophy, and neuromuscular contractures.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Skeletal muscle-specific myostatin overexpression promotes muscle oxidative capacity and fatigue resistance in transgenic mice.Experimental physiology · 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
- Theoretical-Experimental Analysis to Elucidate the Mechanism of Action of Novel Anabolic Agents.Molecules (Basel, Switzerland) · 2025Article
- Sexual dimorphisms in skeletal muscle: current concepts and research horizons.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Review
- The role of sympathetic innervation in neonatal muscle growth and neuromuscular contractures.The FEBS journal · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Neonatal brachial plexus injury (NBPI) causes disabling and incurable muscle contractures that result from impaired longitudinal growth of denervated muscles. This deficit in muscle growth is driven by increased proteasome-mediated protein degradation, suggesting a dysregulation of muscle proteostasis. The myostatin (MSTN) pathway, a prominent muscle-specific regulator of proteostasis, is a putative signaling mechanism by which neonatal denervation could impair longitudinal muscle growth, and thus a potential target to prevent NBPI-induced contractures. Through a mouse model of NBPI, our present study revealed that pharmacologic inhibition of MSTN signaling induces hypertrophy, restores longitudinal growth, and prevents contractures in denervated muscles of female but not male mice, despite inducing hypertrophy of normally innervated muscles in both sexes. Additionally, the MSTN-dependent impairment of longitudinal muscle growth after NBPI in female mice is associated with perturbation of 20S proteasome activity, but not through alterations in canonical MSTN signaling pathways. These findings reveal a sex dimorphism in the regulation of neonatal longitudinal muscle growth and contractures, thereby providing insights into contracture pathophysiology, identifying a potential muscle-specific therapeutic target for contracture prevention, and underscoring the importance of sex as a biological variable in the pathophysiology of neuromuscular disorders.
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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.