Sporadic inclusion-body myositis: A degenerative muscle disease associated with aging, impaired muscle protein homeostasis and abnormal mitophagy.

@article{Askanas2015SporadicIM,
  title={Sporadic inclusion-body myositis: A degenerative muscle disease associated with aging, impaired muscle protein homeostasis and abnormal mitophagy.},
  author={Valerie Askanas and W. King Engel and Anna Nogalska},
  journal={Biochimica et biophysica acta},
  year={2015},
  volume={1852 4},
  pages={
          633-43
        }
}
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81 Citations

Sporadic Inclusion Body Myositis: An Acquired Mitochondrial Disease with Extras
TLDR
It is warranted to regard IBM as a mitochondrial disease, offering a feasible therapeutic target to be developed for this yet untreatable condition.
Sporadic Inclusion Body Myositis: An Acquired Mitochondrial Disease with Extras.
TLDR
Based on the cumulating evidence of mitochondrial abnormality as a disease contributor, it is warranted to regard IBM as a mitochondrial disease, offering a feasible therapeutic target for this yet untreatable condition.
Inclusion body myositis: clinical features and pathogenesis
  • S. Greenberg
  • Biology, Medicine
    Nature Reviews Rheumatology
  • 2019
TLDR
Mounting evidence that IBM is an autoimmune T cell-mediated disease provides hope that future therapies directed towards depleting these cells could be effective and contributes to the mounting evidence arguing for the important pathogenic function of the immune system.
Molecular events linking cholesterol to Alzheimer's disease and inclusion body myositis in a rabbit model.
TLDR
The significant overlap on the changes of gene expression in the brain and muscle of rabbits fed with cholesterol-enriched diet supports the notion that LOAD and sIBM may share a common etiology.
Genetic Investigations of Sporadic Inclusion Body Myositis and Myopathies with Structural Abnormalities and Protein Aggregates in Muscle
TLDR
The collection of a large series of sIBM patients through the IIBMGC has been shown here to reveal important genetic findings and will be a valuable resource for the future.
Immune and myodegenerative pathomechanisms in inclusion body myositis
TLDR
Recent insights into the pathomechanistic network of mutually dependent inflammatory and degenerative events during inclusion Body Myositis are discussed.
Immunohistochemical and ultrastructural analysis of sporadic inclusion body myositis: a case series
TLDR
Using a combination of immunohistochemistry and electron microscopy methods, the correct final diagnosis ofporadic inclusion body myositis is established and a specific treatment is implemented to inhibit disease progression.
Amyloid deposits and inflammatory infiltrates in sporadic inclusion body myositis: the inflammatory egg comes before the degenerative chicken
TLDR
It is imperative that neurologists and rheumatologists recognize this disorder which may, through clinical and pathological similarities, mimic other myopathies, especially polymyositis, which responds to immunosuppressant drug therapy poorly.
Metabolomes of mitochondrial diseases and inclusion body myositis patients: treatment targets and biomarkers
TLDR
The omics approach identified pathways currently used to treat NMDs and mitochondrial stroke‐like episodes and proposes nicotinamide riboside in MDs and IBM, and creatine in IOSCA and IBM as novel treatment targets.
Viruses in IBM
Inclusion body myositis (IBM) is the most common and disabling inflammatory myopathy above age 50 years, with seemingly increasing prevalence and complex pathogenesis.1,2 Cytotoxic-perforin-secreting…
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References

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Pathogenic Considerations in Sporadic Inclusion-Body Myositis, a Degenerative Muscle Disease Associated With Aging and Abnormalities of Myoproteostasis
TLDR
This work reviews the presumably most important known molecular abnormalities that occur in s-IBM myofibers and that likely contribute to s- IBM pathogenesis and suggests interventions in the complex, interwoven pathogenic cascade of s-ibM are suggested.
Inclusion-body myositis
TLDR
It is proposed that the identified abnormal accumulation, misfolding, and aggregation of proteins, perhaps provoked by the aging milieu and aggravated by the oxidative stress, lead to the s-IBM-specific vacuolar degeneration and atrophy of muscle fibers.
Inclusion-body myositis: muscle-fiber molecular pathology and possible pathogenic significance of its similarity to Alzheimer’s and Parkinson’s disease brains
TLDR
Diagnostic criteria is summarized, and it is suggested that the intra-muscle-fiber degenerative component plays the primary role, leading to muscle-Fiber destruction and clinical weakness, since anti-inflammatory treatments are not of sustained benefit.
p62/SQSTM1 is overexpressed and prominently accumulated in inclusions of sporadic inclusion-body myositis muscle fibers, and can help differentiating it from polymyositis and dermatomyositis
TLDR
In s-IBM muscle fibers, p62 protein is increased on both the protein and the mRNA levels, and it is strongly accumulated within, and as a dense peripheral shell surrounding, p-tau containing inclusions, by both the light- and electron-microscopy.
In inclusion-body myositis muscle fibers Parkinson-associated DJ-1 is increased and oxidized.
Does Overexpression of βAPP in Aging Muscle Have a Pathogenic Role and a Relevance to Alzheimer’s Disease? : Clues from Inclusion Body Myositis, Cultured Human Muscle, and Transgenic Mice
Amyloid-β42 is preferentially accumulated in muscle fibers of patients with sporadic inclusion-body myositis
TLDR
It is suggested that Aβ42 oligomers and their cytotoxicity may play an important role in the s-IBM pathogenesis.
Inclusion Body Myositis: A Degenerative Muscle Disease Associated with Intra‐Muscle Fiber Multi‐Protein Aggregates, Proteasome Inhibition, Endoplasmic Reticulum Stress and Decreased Lysosomal Degradation
TLDR
Abnormal intracellular accumulation of unfolded proteins may lead to their aggregation and inclusion body formation, and s‐IBM can be considered a "conformational disorder" caused by protein unfolding/misfolding combined with the formation of inclusion bodies.
Abnormalities of NBR1, a novel autophagy-associated protein, in muscle fibers of sporadic inclusion-body myositis
TLDR
The demonstration of NBR1 abnormalities in s-IBM provides further evidence that altered protein degradation pathways may be critically involved in the s-ibM pathogenesis, and attempts to unblock defective protein degradation might be a therapeutic strategy for s- IBM patients.
Novel demonstration of conformationally modified tau in sporadic inclusion-body myositis muscle fibers
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