ArticleMolecular neurobiology2018
Endoplasmic Reticulum Stress Induces Myostatin High Molecular Weight Aggregates and Impairs Mature Myostatin Secretion.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Alterations in systemic and skeletal muscle myostatin regulation are most prominent at disease onset and associate with muscle-related outcomes in idiopathic inflammatory myopathies.Arthritis research & therapy · 2026Article
- Mitochondrial damage is associated with an early immune response in inclusion body myositis.Brain : a journal of neurology · 2025Article
- Idiopathic Inflammatory Myopathy-Molecular Mechanisms Underlying Its Pathogenesis and Physical Therapy Effects.International journal of molecular sciences · 2025Review
- Sporadic Inclusion Body Myositis at the Crossroads between Muscle Degeneration, Inflammation, and Aging.International journal of molecular sciences · 2024Review
- Mitochondrial defects in sporadic inclusion body myositis-causes and consequences.Frontiers in cell and developmental biology · 2024Review
- Therapeutic Candidates for Alzheimer's Disease: Saponins.International journal of molecular sciences · 2023Review
- Myostatin in idiopathic inflammatory myopathies: Serum assessment and disease activity.Neuropathology and applied neurobiology · 2023Article
- Role of Myokines in Myositis Pathogenesis and Their Potential to be New Therapeutic Targets in Idiopathic Inflammatory Myopathies.Journal of immunology research · 2020Review
- Niban protein regulates apoptosis in HK-2 cells via caspase-dependent pathway.Renal failure · 2019Article
- Fibril-induced glutamine-/asparagine-rich prions recruit stress granule proteins in mammalian cells.Life science alliance · 2019Article
- Inclusion Body Myositis: Update on Pathogenesis and Treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
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Authors and funding
9 authors.
Funding
Abstract
Sporadic inclusion body myositis (sIBM) is the most prevalent acquired muscle disorder in the elderly with no defined etiology or effective therapy. Endoplasmic reticulum stress and deposition of myostatin, a secreted negative regulator of muscle growth, have been implicated in disease pathology. The myostatin signaling pathway has emerged as a major target for symptomatic treatment of muscle atrophy. Here, we systematically analyzed the maturation and secretion of myostatin precursor MstnPP and its metabolites in a human muscle cell line. We find that increased MsntPP protein levels induce ER stress. MstnPP metabolites were predominantly retained within the endoplasmic reticulum (ER), also evident in sIBM histology. MstnPP cleavage products formed insoluble high molecular weight aggregates, a process that was aggravated by experimental ER stress. Importantly, ER stress also impaired secretion of mature myostatin. Reduced secretion and aggregation of MstnPP metabolites were not simply caused by overexpression, as both events were also observed in wildtype cells under ER stress. It is tempting to speculate that reduced circulating myostatin growth factor could be one explanation for the poor clinical efficacy of drugs targeting the myostatin pathway in sIBM.
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