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Tytuł:
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Mitochondrial dysfunction in anti-3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) immune-mediated necrotising myopathy.
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Autorzy:
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Acosta IJ; Neuropathology Department, John Radcliffe Hospital, Oxford University Hospitals Trust, Oxford, OX3 9DU, United Kingdom; Translational neurology and neurophysiology laboratory. Advance clinical research centre (CICA), School of Medicine, Universidad de Chile, Providencia, Santiago 7500787, Chile; Neurology and Psychiatry department, Clínica Alemana Santiago, Vitacura 5951, Vitacura, Santiago 7650568, Chile; Neurology and Neurosurgery department, Clínica Dávila, Recoleta, Santiago 8531657, Chile. Electronic address: .
Hofer M; Neuropathology Department, John Radcliffe Hospital, Oxford University Hospitals Trust, Oxford, OX3 9DU, United Kingdom.
Brady S; Oxford Muscle Service, Department of Neurology, John Radcliffe Hospital, Oxford University Hospitals Trust, Oxford OX3 9DU, United Kingdom.
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Źródło:
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Neuromuscular disorders : NMD [Neuromuscul Disord] 2022 May; Vol. 32 (5), pp. 441-444. Date of Electronic Publication: 2022 Mar 25.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: Oxford ; New York : Pergamon Press, c1991-
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MeSH Terms:
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Autoimmune Diseases*/pathology
Hydroxymethylglutaryl-CoA Reductase Inhibitors*
Muscular Diseases*/pathology
Myositis*/pathology
Autoantibodies ; Case-Control Studies ; Coenzymes ; Humans ; Hydroxymethylglutaryl CoA Reductases ; Mitochondria/pathology ; Muscle, Skeletal/pathology ; Necrosis/pathology
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Contributed Indexing:
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Keywords: HMGCR; Mitochondria; Muscle biopsy; Myositis
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Substance Nomenclature:
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0 (Autoantibodies)
0 (Coenzymes)
0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
EC 1.1.1.- (HMGCR protein, human)
EC 1.1.1.- (Hydroxymethylglutaryl CoA Reductases)
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Entry Date(s):
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Date Created: 20220429 Date Completed: 20220517 Latest Revision: 20220706
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Update Code:
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20240105
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DOI:
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10.1016/j.nmd.2022.03.005
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PMID:
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35487868
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Mitochondrial dysfunction is a plausible cause of muscle fibre damage in a number of myopathies including immune-mediated necrotising myopathy. However, histopathological evidence of mitochondrial dysfunction is not often described in immune-mediated necrotising myopathy and, when present, it is often attributed to patient age. The purpose of this study was to describe features of mitochondrial dysfunction on muscle biopsy in anti-3‑hydroxy-3-methylglutaryl-CoA reductase immune-mediated necrotising myopathy and explore whether these features are age-related. In this observational case control study, a statistically significant increase in the number of muscle fibres with increased lipid content (p = 0.004) and cytochrome c oxidase-negative/succinate dehydrogenase-positive fibres (p = 0.037) in anti-3‑hydroxy-3-methylglutaryl-coenzyme immune-mediated necrotising myopathy was found compared to age-matched controls. Therefore, histopathological features of mitochondrial dysfunction are more frequent in anti-3‑hydroxy-3-methylglutaryl-coenzyme immune-mediated necrotising myopathy than aged-matched controls and therefore, may be contributing to the pathogenesis.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Crown Copyright © 2022. Published by Elsevier B.V. All rights reserved.)
