Inclusion-body myositis, a multifactorial muscle disease associated with aging: current concepts of pathogenesis
@article{Askanas2007InclusionbodyMA, title={Inclusion-body myositis, a multifactorial muscle disease associated with aging: current concepts of pathogenesis}, author={Valerie Askanas and W. King Engel}, journal={Current Opinion in Rheumatology}, year={2007}, volume={19}, pages={550–559} }
Purpose of reviewSporadic inclusion-body myositis, the most common muscle disease of older persons, has no known cause or persistently beneficial treatment. The unfolding pathogenesis could lead to new treatment strategies and it is now of growing interest among clinicians and basic scientists. About 100 papers related to the subject were published in 2006 and the first part of 2007 (we cite only articles most relevant to this review). Recent findingsThis review focuses on the current concepts…
90 Citations
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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.
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This article summarizes the most recent findings leading to better understanding of the players in the pathogenetic cascade and suggests that lymphocytic inflammatory component is probably secondary, and it may contribute only slightly to muscle fiber damage in sporadic inclusion-body myositis.
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The basic hypothesis is that overexpression of AβPP within the aging muscle fibers is an early upstream event causing a subsequent pathogenic cascade that leads to sporadic inclusion‐body myositis.
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Transgenic mice were derived in which selective overexpression of βAPP leads to the development of a subset of other histopathological and clinical features characteristic of IBM, including centric nuclei, inflammation, and deficiencies in motor performance, consistent with a pathogenic role for βAPP mismetabolism in human IBM.
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Muscle biopsies from patients with sporadic inclusion-body myositis (sIBM) consistently demonstrate that the inflammatory T cells almost invariably invade intact (not vacuolated) fibers, whereas the…
Myostatin is increased and complexes with amyloid-β within sporadic inclusion-body myositis muscle fibers
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It is suggested that myostatin/myostatin precursor, either alone, or bound to Aβ, may play a novel role in the pathogenesis of s-IBM.