ReviewJournal of neuromuscular diseases2024
Contribution of Complement, Microangiopathy and Inflammation in Idiopathic Inflammatory Myopathies.
Review in Journal of neuromuscular diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 10 citations in OpenAlex.
- Glycoproteomic Signatures of IgG SubclassMedComm · 2026Article
- Myovascular Niche: The Role of Endothelial Cells in Skeletal Muscle Health and Disease.Circulation research · 2026Review
- Emerging therapies in idiopathic inflammatory myopathies.Journal of neuromuscular diseases · 2026Review
- The evolving landscape of complement therapeutics in rheumatology.Annals of the rheumatic diseases · 2026Review
- Tetrandrine-based in situ vaccination via multifunctional Mn²⁺-hyaluronic acid hydrogel loading gelatinase-responsive nanoparticles.Journal of nanobiotechnology · 2026Article
- Myxovirus Resistance A Protein Expression in Idiopathic Inflammatory Myopathies and Hereditary Muscle Diseases with Inflammatory Cell Infiltration: A North African Study.International journal of molecular sciences · 2026Article
- Convergent innate immune and regulated cell-death pathways in selected myopathies.Frontiers in immunology · 2026Review
- Atypical dermatomyositis with positive anti-nuclear matrix protein 2 antibodies complicated by rhabdomyolysis syndrome: a case report and literature review.Frontiers in immunology · 2026Review
- Autoimmune Neuromuscular Disorders at a Molecular Crossroad: Linking Pathogenesis to Targeted Immunotherapy.International journal of molecular sciences · 2025Review
- Immune-Mediated Necrotizing Myopathy: A Systematic Review of Antibody-Specific Mechanisms and Treatment Outcomes.Cureus · 2025Review
- Review
- Calcinosis in dermatomyositis.Current opinion in rheumatology · 2024Review
- Advances in Juvenile Dermatomyositis: Pathophysiology, Diagnosis, Treatment and Interstitial Lung Diseases-A Narrative Review.Children (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewIdiopathic inflammatory myopathies (IIMs) are a heterogeneous group characterized by muscle weakness and skin symptoms and are categorized into six subtypes: dermatomyositis (DM), polymyositis (PM), anti-synthetase syndrome (ASS), immune-mediated myopathy (IMNM), inclusion body myopathy (IBM), and overlap myositis. Myositis-specific autoantibodies were detected for the diagnosis and classification of IIM. This review highlights the pathogenic contributions of the complement system, microangiopathy, and inflammation in IIM. RECENT
findingsDeposition of complement around capillaries and/or the sarcolemma was observed in muscle biopsy specimens from patients with DM, ASS, and IMNM, suggesting the pathomechanism of complement-dependent muscle and endothelial cell injury. A recent study using human muscle microvascular endothelial cells showed that Jo-1 antibodies from ASS induce complement-dependent cellular cytotoxicity in vitro. Based on both clinical and pathological observations, antibody- and complement-mediated microangiopathy may contribute to the development of DM and anti-Jo-1 ASS. Juvenile DM is characterized by the loss of capillaries, perivascular inflammation, and small-vessel angiopathies, which may be related to microinfarction and perifascicular atrophy. Several serum biomarkers that reflect the IFN1 signature and microangiopathy are elevated in patients with DM. The pathological observation of myxovirus resistance protein A (MxA), which suggests a type 1 interferon (IFN1) signature in DM, supports the diagnosis and further understanding of the pathomechanism of IIM. A recent report showed that an increase in triggering receptor expressed on myeloid cells (TREM-1) around perimysial blood vessels and muscles in patients with IIM plays a role in triggering inflammation and promoting the migration of inflammatory cells by secreting proinflammatory cytokines, such as tumor necrosis factor α. SUMMARY: The deposition of complement in muscles and capillaries is a characteristic feature of DM, ASS, and IMNM. Microangiopathy plays a pathogenic role in DM, possibly resulting in perifascicular atrophy. Further understanding of the detailed pathomechanism regarding complement, microangiopathy, and inflammation may lead to novel therapeutic approaches for IIM.
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