ArticleJournal of neurology2025
Mitochondrial pathology in inflammatory myopathies: a marker of worse clinical outcome.
Article in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Energy metabolism dysregulation in idiopathic inflammatory myopathies: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Late-Onset Multiple Acyl-CoA Dehydrogenase Deficiency (MADD): Clinical Features, Diagnostic Challenges, and the Role of Oxidative Stress in Pathophysiology.Antioxidants (Basel, Switzerland) · 2025Article
- Myopathology and Immune Profile of Granulomatous Myositis in Sarcoid Myopathy.Neuropathology and applied neurobiology · 2025Article
- Idiopathic Inflammatory Myopathy-Molecular Mechanisms Underlying Its Pathogenesis and Physical Therapy Effects.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesMitochondrial dysfunction is well documented in inclusion body myositis (IBM), but its role in non-IBM myositis remains unclear. This study aimed to investigate the prevalence and clinical significance of mitochondrial pathology in non-IBM myositis and to assess its potential role as a marker for disease progression towards IBM, treatment response, and clinical outcomes.
methodsMuscle biopsies from 850 patients with inflammatory myopathy (IM) across 6 neuromuscular centers in Italy, France, and Germany were retrospectively analyzed. Inclusion required meeting diagnostic criteria for definite adult IM, mitochondrial pathology (age-exceeding numbers of COX-negative fibers), and exclusion of definite IBM according to Hilton-Jones 2013 criteria. The percentage of COX-negative fibers was quantified, correlated with clinical outcomes, and compared with myositis control cases without relevant signs of mitochondrial alterations.
resultsTwenty-five patients with non-IBM myositis and mitochondrial abnormalities were identified. These patients, predominantly women (68%), had a mean onset age of 58.8 years. Polymyositis with mitochondrial pathology (PM-Mito) and nonspecific myositis (NSM) were the most prevalent subtypes (72%). The mean percentage of COX-negative fibers was 3% (0.25-8.5%) in these patients. The presence of mitochondrial pathology was associated with treatment refractoriness and worse clinical outcome evaluated based on residual muscle weakness and the level of independence (p < 0.005). A higher percentage of COX-negative fibers also correlated with poorer clinical outcomes (p = 0.031). Four patients, initially diagnosed with PM-Mito and NSM, progressed to definite IBM.
conclusionsMitochondrial dysfunction represents a key element informing about disease severity and poor clinical outcomes in non-IBM myositis. It may predict progression to IBM, especially in PM-Mito and NSM, and guide treatment strategies.
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