ReviewCurrent opinion in neurology2010
Sporadic inclusion body myositis: possible pathogenesis inferred from biomarkers.
Review in Current opinion in neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 51 citations in OpenAlex.
- Influence of Inflammatory Cytokines IL-1Mediators of inflammation · 2023Article
- Review
- A metastable subproteome underlies inclusion formation in muscle proteinopathies.Acta neuropathologica communications · 2019Article
- ULK2 is essential for degradation of ubiquitinated protein aggregates and homeostasis in skeletal muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Immunohistochemical and ultrastructural analysis of sporadic inclusion body myositis: a case series.Rheumatology international · 2019Article
- Proteomics of rimmed vacuoles define new risk allele in inclusion body myositis.Annals of neurology · 2017Article
- Development and evaluation of a standardized ELISA for the determination of autoantibodies against cN-1A (Mup44, NT5C1A) in sporadic inclusion body myositis.Auto- immunity highlights · 2016Article
- Disease specificity of autoantibodies to cytosolic 5'-nucleotidase 1A in sporadic inclusion body myositis versus known autoimmune diseases.Annals of the rheumatic diseases · 2016Article
- T-Cell-Mediated Inflammatory Myopathies in HIV-Positive Individuals: A Histologic Study of 19 Cases.Journal of neuropathology and experimental neurology · 2016Article
- PFKM gene defect and glycogen storage disease GSDVII with misleading enzyme histochemistry.Neurology. Genetics · 2015Article
- Targeted sequencing and identification of genetic variants in sporadic inclusion body myositis.Neuromuscular disorders : NMD · 2015Article
- Expression of FSHD-related DUX4-FL alters proteostasis and induces TDP-43 aggregation.Annals of clinical and translational neurology · 2015Article
- Inclusion body myositis - pathomechanism and lessons from genetics.Open medicine (Warsaw, Poland) · 2015Review
- Emerging therapeutic options for sporadic inclusion body myositis.Therapeutics and clinical risk management · 2015Review
- Proteasome dysfunction induces muscle growth defects and protein aggregation.Journal of cell science · 2014Article
- Ongoing developments in sporadic inclusion body myositis.Current rheumatology reports · 2014Review
- Sporadic inclusion body myositis: new insights and potential therapy.Current opinion in neurology · 2014Article
- Gene expression profiling in tibial muscular dystrophy reveals unfolded protein response and altered autophagy.PloS one · 2014Article
- Update in inclusion body myositis.Current opinion in rheumatology · 2013Review
- Comparative utility of LC3, p62 and TDP-43 immunohistochemistry in differentiation of inclusion body myositis from polymyositis and related inflammatory myopathies.Acta neuropathologica communications · 2013Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
purpose of reviewThe relevance of proteins that accumulate and aggregate in the muscle fibers of patients with sporadic inclusion body myositis (sIBM) is unknown. Many of these proteins also aggregate in other disorders, including Alzheimer's disease, leading to speculation that sIBM pathogenesis has similarities to neurodegenerative disorders. Our review will discuss current studies on these protein biomarkers and their utility in sIBM diagnosis. RECENT
findingsTwo 'classical' components of sIBM aggregates (amyloid beta and phospho-tau) have been re-evaluated. Three additional components of aggregates (TDP-43, p62, and LC3) have been identified. The sensitivity and specificity of these biomarkers has been explored. Two studies suggest that TDP-43 may have clinical utility in distinguishing sIBM from other inflammatory myopathies. SUMMARY: The fact that sIBM muscle accumulates multiple protein aggregates with no single protein appearing in every sIBM patient biopsy suggests that it is not presently possible to place pathogenic blame on any single protein (i.e. amyloid beta or TDP-43). Instead changes in protein homeostasis may lead to the accumulation of different proteins that have a propensity to aggregate in skeletal muscle. Therapies aimed at improving protein homeostasis, instead of targeting a specific protein that may or may not accumulate in all sIBM patients, could be useful future strategies for this devastating and enigmatic disorder.
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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.