ArticleProteome science2014
Proteomic study of sporadic inclusion body myositis.
Article in Proteome science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Spatial protein expression patterns across pathologically-associated fibers revealed molecular specialization in inclusion body myositis.Cell communication and signaling : CCS · 2026Article
- Ageing-Associated Dysregulation of Myogenic Differentiation in Inclusion Body Myositis.Journal of cachexia, sarcopenia and muscle · 2026Review
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- Sporadic Inclusion Body Myositis at the Crossroads between Muscle Degeneration, Inflammation, and Aging.International journal of molecular sciences · 2024Review
- APP in the Neuromuscular Junction for the Development of Sarcopenia and Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Endoplasmic Reticulum Stress Induces Myostatin High Molecular Weight Aggregates and Impairs Mature Myostatin Secretion.Molecular neurobiology · 2018Article
- Calcium dysregulation, functional calpainopathy, and endoplasmic reticulum stress in sporadic inclusion body myositis.Acta neuropathologica communications · 2017Article
- Proteomics of rimmed vacuoles define new risk allele in inclusion body myositis.Annals of neurology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSporadic inclusion body myositis (s-IBM) is the most commonly occurring acquired inflammatory myopathy in elderly people (>45 years); however, pathogenic mechanisms are poorly understood and diagnostic tools are limited. In view of this, new therapeutic and diagnostic molecular markers for s-IBM need to be identified. EXPERIMENTAL
designIn this study, the proteomes from three s-IBM cases were compared with those from three cases of neurogenic muscular atrophy (control). Proteins were separated by 2-dimensional polyacrylamide gel electrophoresis and profiled by mass spectrometric sequencing and subsequently validated by western blot.
resultsDifferential expression was noted in 29 proteins (16 upregulated and 13 downregulated) in s-IBM compared with the control group. Functions of these proteins include oxidative stress response, regulation of apoptosis, signal transduction, and cytoskeleton. Expression of both amyloid precursor protein (APP) and αB-crystallin was increased in s-IBM cases.
conclusionsOur study reveals a unique pattern of protein expression in s-IBM, which should be further investigated in a wider cohort of IBM patients to fully realize the potential diagnostic or therapeutic benefits.
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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.