ArticleNature communications2024
IFNγ causes mitochondrial dysfunction and oxidative stress in myositis.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed.
- Juvenile Myositis: Insights on Classification, Pathogenesis, and Therapies Over the Past 50 Years.Arthritis care & research · 2026Review
- Myopathies in clinical care: a focus on treatable causes.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Mitochondrial RNA-Type I Interferon Axis in Sjögren's Disease: Molecular Mechanisms and Translational Implications.International journal of molecular sciences · 2026Review
- The Role of Inflammation and Immunity in Cardiovascular Disease: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Dysregulated IL-6 pathway activity in idiopathic inflammatory myopathies.Arthritis research & therapy · 2026Article
- Emerging therapies in idiopathic inflammatory myopathies.Journal of neuromuscular diseases · 2026Review
- Interferon-elicited lipoprotein metabolism in lung fibroblasts facilitates premetastatic niche formation.Nature communications · 2026Article
- LPAR4 mediates resistance to interferon-induced stress in soft tissue sarcoma.Science advances · 2026Article
- Interplay between sarcopenia and type 2 diabetes: mechanisms, implications, and therapeutic prospects.Nutrition & diabetes · 2026Review
- Mitochondrial drivers of stem cell aging and inflammaging.npj aging · 2026Review
- Etiopathogenesis of Immune-Mediated Necrotizing Myopathy: A Comprehensive Review of Recent Advances.CNS neuroscience & therapeutics · 2026Review
- Gastrodin Ameliorates Pain-Depression Comorbidity through SIRT3-Dependent Alleviation of Oxidative Stress and Promotion of Mitochondrial Biogenesis.Molecular neurobiology · 2026Article
- Ageing-Associated Dysregulation of Myogenic Differentiation in Inclusion Body Myositis.Journal of cachexia, sarcopenia and muscle · 2026Review
- The ageing microenvironment in sarcopenia: early alterations and targeted therapeutic strategies.Frontiers in immunology · 2026Review
- The inflammatory clock: how cGAS-STING ticks in the aging ovary.Frontiers in cell and developmental biology · 2026Review
- Energy metabolism dysregulation in idiopathic inflammatory myopathies: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Digitally Assessed Long COVID Symptomatology Is Associated With Lymphocyte Mitochondrial Dysfunction and Altered Immune Potential.Open forum infectious diseases · 2025Article
- Myopathology and Immune Profile of Granulomatous Myositis in Sarcoid Myopathy.Neuropathology and applied neurobiology · 2025Article
- Preclinical efficacy of adipose-derived cell therapies for the treatment of myositis.Stem cells translational medicine · 2025Article
- Mitochondria and lysosomes in T cell immunometabolism.Trends in immunology · 2025Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Idiopathic inflammatory myopathies (IIMs) are severe autoimmune diseases with poorly understood pathogenesis and unmet medical needs. Here, we examine the role of interferon γ (IFNγ) using NOD female mice deficient in the inducible T cell co-stimulator (Icos), which have previously been shown to develop spontaneous IFNγ-driven myositis mimicking human disease. Using muscle proteomic and spatial transcriptomic analyses we reveal profound myofiber metabolic dysregulation in these mice. In addition, we report muscle mitochondrial abnormalities and oxidative stress in diseased mice. Supporting a pathogenic role for oxidative stress, treatment with a reactive oxygen species (ROS) buffer compound alleviated myositis, preserved muscle mitochondrial ultrastructure and respiration, and reduced inflammation. Mitochondrial anomalies and oxidative stress were diminished following anti-IFNγ treatment. Further transcriptomic analysis in IIMs patients and human myoblast in vitro studies supported the link between IFNγ and mitochondrial dysfunction observed in mice. These results suggest that mitochondrial dysfunction, ROS and inflammation are interconnected in a self-maintenance loop, opening perspectives for mitochondria therapy and/or ROS targeting drugs in myositis.
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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.