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Objectives: Anti-signal recognition particle (SRP) antibodies, markers of immune-mediated necrotising myopathy, are reportedly related to cardiac involvement; however, whether they are pathogenic to the myocardium remains unclear. We aimed, therefore, to explore the pathogenicity of anti-SRP antibodies against the myocardium through and studies.
Methods: Total immunoglobulin G (IgG), purified from patients with positive anti-SRP antibodies, was passively transferred into C57BL/6 mice. Cardiac function was evaluated via echocardiography and the ventricular pressure-volume loop; cardiac histological changes were analysed using haematoxylin-eosin staining, picrosirius red staining, immunofluorescence and immunohistochemistry. Additionally, reactive oxygen species (ROS) formation was evaluated by dihydroethidium (DHE) staining; mitochondrial morphology and function were evaluated using transmission electron microscopy and seahorse mitochondrial respiration assay, respectively. The myositis cohort at our centre was subsequently reviewed in terms of cardiac assessments.
Results: After the passive transfer of total IgG from patients with positive anti-SRP antibodies, C57BL/6 mice developed significant left ventricular diastolic dysfunction (LVDD). Transcriptomic analysis and corresponding experiments revealed increased oxidative stress and mitochondrial damage in the hearts of the experimental mice. Cardiomyocytes exposed to anti-SRP-specific IgG, however, recovered normal mitochondrial metabolism after treatment with N-acetylcysteine, an ROS scavenger. Moreover, patients positive for anti-SRP antibodies manifested worse diastolic but equivalent systolic function compared to their counterparts after propensity score matching.
Conclusion: Anti-SRP antibodies may play a pathogenic role in the development of LVDD by promoting ROS production and subsequent myocardial mitochondrial impairment. The inhibition of oxidative stress was effective in reversing anti-SRP antibody-induced LVDD.
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http://dx.doi.org/10.1002/cti2.1525 | DOI Listing |
Fukushima J Med Sci
December 2024
Department of Rheumatology, Fukushima Medical University School of Medicine.
Myositis-specific autoantibodies play an important role on the disease phenotype of idiopathic inflammatory myopathies (IIMs). Anti-signal recognition particle (SRP) antibody-positive patients with IIMs may present with severe myopathy and highly elevated serum creatine kinase levels. These patients are often resistant to immunosuppressive therapy, but there is no established treatment strategy.
View Article and Find Full Text PDFMedicina (Kaunas)
October 2024
Faculty of Medicine, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.
ACR Open Rheumatol
November 2024
Johns Hopkins University School of Medicine, Baltimore, Maryland.
Objective: Idiopathic inflammatory myopathies (IIMs) are a group of heterogeneous, systemic autoimmune diseases characterized by specific clinical features and, frequently, skeletal muscle inflammation. Specific subtypes of IIMs can be characterized by myositis-specific autoantibodies and are associated with distinct clinical phenotypes. Here, we focus on anti-melanoma differentiation-associated protein 5 (MDA5)-positive myositis and anti-signal recognition particle (SRP)-positive myositis, both of which exhibit seasonality but lack known environmental triggers.
View Article and Find Full Text PDFFront Immunol
November 2024
Department of Neurology, Peking University First Hospital, Beijing, China.
Objective: We aimed to explore the efficacy and safety of efgartigimod in patients with refractory immune-mediated necrotizing myopathy (IMNM).
Methods: This open-label pilot observational study included seven patients with refractory IMNM, all of whom received intravenous efgartigimod treatment. The clinical response was assessed after 4 weeks of efgartigimod treatment according to the 2016 American College of Rheumatology-European League Against Rheumatism response criteria for adult idiopathic inflammatory myopathy.
Cureus
September 2024
Department of Respiratory Medicine, Fukuchiyama City Hospital, Kyoto, JPN.
Immune-mediated necrotizing myopathy (IMNM), an inflammatory muscle disease, typically presents as severe muscle weakness due to immunologic mechanisms. Some cases also show cutaneous manifestations, interstitial lung disease, and sicca symptoms. In this report, we present a unique case of an elderly man with a history of mild and stable Sjögren's syndrome (SS) for over 10 years, who later developed interstitial lung disease and myositis, leading to a diagnosis of IMNM confirmed by the presence of anti-signal recognition particle antibodies.
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