ReviewRheumatology (Oxford, England)2025
Inclusion body myositis and immunosenescence: current evidence and future perspectives.
Review in Rheumatology (Oxford, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy and safety of pharmacological treatments in inclusion body myositis: a systematic review.RMD open · 2025Pooled it
- Immunosenescence and organoids: pathophysiology and therapeutic opportunities.Immunity & ageing : I & A · 2025Review
- Integrative Approaches to Myopathies and Muscular Dystrophies: Molecular Mechanisms, Diagnostics, and Future Therapies.International journal of molecular sciences · 2025Review
- Advances in the Regulation by Immune Cells of Skeletal Myositis Outcomes.Aging and disease · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
IBM remains an enigmatic and complex muscle disorder where a deeper understanding of disease pathomechanisms and the identification of potential genetic contributors represent an unmet need. The absence of effective treatments has spurred endeavours to reassess the interplay between degeneration, including autophagy, mitochondrial dysfunction and proteasomal dysregulation, and autoimmunity. IBM is unique among the other idiopathic inflammatory myopathies owing to its molecular signature involving highly differentiated cytotoxic T cells that evade immune regulation. This has led to a resurgence of interest in the development of immunomodulatory therapy. This review discusses the potential role of cellular immunosenescence in sustaining inflammation and/or fibrotic remodelling observed in IBM and appraises the rationale for some potential therapeutic approaches to mitigate disease progression.
Indexed as
Identifiers
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.