ReviewCurrent opinion in rheumatology2010
Novel therapeutic approaches for inclusion body myositis.
Review in Current opinion in rheumatology, 2010. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
8 citing papers in PubMed, 17 citations in OpenAlex.
- Phosphorylated TDP-43 (pTDP-43) aggregates in the axial skeletal muscle of patients with sporadic and familial amyotrophic lateral sclerosis.Acta neuropathologica communications · 2018Article
- Reply to Letter to the Editor.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Tdp-43 cryptic exons are highly variable between cell types.Molecular neurodegeneration · 2017Article
- Inclusion body myositis - pathomechanism and lessons from genetics.Open medicine (Warsaw, Poland) · 2015Review
- 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
- Myostatin--the holy grail for muscle, bone, and fat?Current osteoporosis reports · 2013Review
- Inclusion body myositis: therapeutic approaches.Degenerative neurological and neuromuscular disease · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
purpose of reviewThis review will highlight recent advances in developing strategies to accelerate muscle regeneration and to slow muscle degeneration in myositis, focusing primarily on inclusion body myositis (IBM). RECENT
findingsTherapies for accelerating muscle regeneration, primarily through inhibition of myostatin, have shown promise in the laboratory and are now entering clinical trials. Recent studies have implicated autophagy, a key cellular process involved in clearance of ubiquitinated aggregates, in the pathogenesis of familial and sporadic inclusion body myositis (sIBM). IBM has joined a growing list of diseases known as TDP-43 proteinopathies, in which this protein becomes mislocalized to the cytoplasm; however, it is unclear whether these protein aggregates or others are pathogenic in this disease. SUMMARY: New discoveries of biomarkers in sIBM and new insights into the pathogenesis of familial IBM are opening novel therapeutic pathways for these disorders. In particular, drugs that stimulate autophagy, already in development for cancer and neurodegenerative diseases, are candidates for clinical trials. These disease-specific therapies combined with novel therapies to accelerate muscle regeneration hold promise for future therapy for this devastating disease.
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What OpenQuestion holds
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.