ArticleActa neuropathologica communications2026
Proteomic profiles in inclusion body myositis and polymyositis with mitochondrial pathology.
Article in Acta neuropathologica communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Mitochondrial dysfunction in neurology: biomarkers and clinical implications.Nature reviews. Neurology · 2026Review
- High-plex spatial protein profiling of skeletal muscle biopsies in inflammatory myopathies using the MACSima™ imaging platform: A pilot study.Acta neuropathologica communications · 2026Article
- Energy metabolism dysregulation in idiopathic inflammatory myopathies: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
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23 authors.
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Abstract
backgroundIdiopathic inflammatory myopathies (IIMs) are autoimmune muscle diseases with distinct clinical, histopathological, and molecular features. Among them, inclusion body myositis (IBM) is refractory to immunotherapy and characterized by combined inflammatory and degenerative changes. Polymyositis with mitochondrial pathology (PM-Mito) has been proposed as a prodromal stage of IBM, but molecular profile underlying this spectrum remains poorly defined.
methodsSkeletal muscle biopsies from 38 IBM, 14 PM-Mito, 5 anti-synthetase syndrome (ASyS), 3 dermatomyositis (DM), 5 immune-mediated necrotizing myopathy (IMNM), and 7 non-diseased controls (NDC) were analyzed by label-free mass spectrometry and validated by bulk RNA sequencing. Dimensionality reduction was performed using sparse Partial Least Squares Discriminant Analysis (sPLS-DA), followed by differential protein analysis.
resultsIBM exhibited a homogeneous and distinct proteomic signature compared with other IIM subtypes, driven by upregulation of MHC class I (e.g. HLA-A) and II (e.g. HLA-DRB1, CD74) molecules, and cytoskeletal proteins (e.g. PDCL3). Comparing IBM to other types of IIM, we also detected increased level of specific histone variants (e.g. HIST2H2AA3, H1FX). Enrichment analysis of the differential proteins underscored increased antigen presentation and T-cell–mediated immunity pathways, with concomitant depletion of mitochondrial respiratory chain, RNA processing, and oxidative phosphorylation components in IBM. PM-Mito shared a proteomic profile with IBM with reduced MT-ND2 levels and increases in lipid storage regulator PLIN1 and extracellular matrix protein COL14A1, among others. In contrast to IBM, PM-Mito preserved type 2 myofiber markers (e.g. MYH2). A specific protein change to PM-Mito was an increase in the cytochrome c oxidase subunit III (MT-CO3), implicating mitochondrial remodelling. Transcriptomic analysis validated the proteomic changes in COL14A1, IGLL4, PLIN1, MT-ND2, SMDT1, and TIMM21, all of which were shared between IBM and PM-Mito.
conclusionIBM exhibits a unique proteomic landscape distinct from other IIMs. The overlap with PM-Mito suggests that these conditions share molecular features, supporting an interpretation that places PM-Mito in the broader spectrum of IBM. Novel protein markers, including histone variants and cytoskeletal regulators, highlight potential pathways for future research. These findings underscore the need for longitudinal studies exploring therapeutic targets in early disease stages.
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