ArticleLaboratory investigation; a journal of technical methods and pathology2019
Association between TDP-43 and mitochondria in inclusion body myositis.
Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- AI-driven predictive modeling of sarcopenia progression in limbic-predominant age-related TDP-43 encephalopathy: a novel biomarker fusion approach.Annals of medicine and surgery (2012) · 2026Article
- The clinical, serological and myopathological features of a cohort of Chinese patients with inclusion body myositis: a single center analysis.Frontiers in immunology · 2026Article
- Mitochondrial damage is associated with an early immune response in inclusion body myositis.Brain : a journal of neurology · 2025Article
- The emerging role of growth differentiation factor 15 as a potential disease biomarker in juvenile dermatomyositis.Rheumatology (Oxford, England) · 2025Article
- Current biomarkers in inclusion body myositis.Journal of neuromuscular diseases · 2024Review
- Inclusion body myositis, viral infections, and TDP-43: a narrative review.Clinical and experimental medicine · 2024Review
- Mitochondrial defects in sporadic inclusion body myositis-causes and consequences.Frontiers in cell and developmental biology · 2024Review
- Cytotoxic immune cells do not affect TDP-43 and p62 sarcoplasmic aggregation but influence TDP-43 localisation.Scientific reports · 2023Article
- The Emerging Role of Mitochondrial Dysfunction in the Pathogenesis of Idiopathic Inflammatory Myopathies.Rambam Maimonides medical journal · 2023Review
- Influence of Inflammatory Cytokines IL-1Mediators of inflammation · 2023Article
- Inclusion Body Myositis and Neoplasia: A Narrative Review.International journal of molecular sciences · 2022Review
- Review
- Feeder-supported in vitro exercise model using human satellite cells from patients with sporadic inclusion body myositis.Scientific reports · 2022Article
- Expanding the TDP-43 Proteinopathy Pathway From Neurons to Muscle: Physiological and Pathophysiological Functions.Frontiers in neuroscience · 2022Review
- Vitamin B12 Reduces TDP-43 Toxicity by Alleviating Oxidative Stress and Mitochondrial Dysfunction.Antioxidants (Basel, Switzerland) · 2021Article
- Mitochondrion-Dependent Cell Death in TDP-43 Proteinopathies.Biomedicines · 2021Review
- Mitophagy and the Brain.International journal of molecular sciences · 2020Review
- Cytoplasmic mislocalization and mitochondrial colocalization of TDP-43 are common features between normal aged and young mice.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Maintaining the balance of TDP-43, mitochondria, and autophagy: a promising therapeutic strategy for neurodegenerative diseases.Translational neurodegeneration · 2020Review
- Why TDP-43? Why Not? Mechanisms of Metabolic Dysfunction in Amyotrophic Lateral Sclerosis.Neuroscience insights · 2020Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Inclusion body myositis (IBM) is the most common cause of primary myopathy in individuals aged 50 years and over, and is pathologically characterized by protein aggregates of p62 and mislocalized cytoplasmic TDP-43, as well as mitochondrial abnormalities in affected muscle fibers. Our recent studies have shown the accumulation of TDP-43 in mitochondria in neurons from patients with amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD), and revealed mitochondria as critical mediators of TDP-43 neurotoxicity. In this study, we investigated the association between mitochondria and TDP-43 in biopsied skeletal muscle samples from IBM patients. We found that IBM pathological markers TDP-43, phosphorylated TDP-43, and p62 all coexisted with intensively stained key subunits of mitochondrial oxidative phosphorylation complexes I-V in the same skeletal muscle fibers of patients with IBM. Further immunoblot analysis showed increased levels of TDP-43, truncated TDP-43, phosphorylated TDP-43, and p62, but decreased levels of key subunits of mitochondrial oxidative phosphorylation complexes I and III in IBM patients compared to aged matched control subjects. This is the first demonstration of the close association of TDP-43 accumulation with mitochondria in degenerating muscle fibers in IBM and this association may contribute to the development of mitochondrial dysfunction and pathological protein aggregates.
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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.