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Tofacitinib Repairs GM-CSF-induced RA Mitochondrial Dysfunction

GSE288373 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2026/04/08 Platform GPL34284Platform GPL24676
Summary
Rheumatoid arthritis (RA) is an autoimmune disease in which synovial tissue macrophages (MΦs) are the primary producer of inflammatory factors. RA synovial MΦ expansion is strongly linked to ultrasound-detected hypertrophy and pathology, and their frequency is 25-fold upregulated during a flare. Consequently, infiltrating MΦs sense and respond to the RA synovial tissue's high energy and oxygen demands. Thus, understanding how hypoxic RA MΦs experience changes in metabolic activity and mitochondrial remodeling will unravel novel therapeutic strategies. Intriguingly, we found that granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulates an RA MΦ inflammatory profile associated with mitochondrial oxidative stress. This study utilized RNA-seq to investigate the effect of GM-CSF treatment on global gene expression changes in MΦs derived from the peripheral blood of rheumatoid arthritis patients.
Published in
Tofacitinib repairs inflammation and mitochondrial dysregulation in GM-CSF-reprogrammed RA macrophages
Satoeya N, Zack SR, Zoubi OA et al. · Cellular & molecular immunology 2026 · PMID 41781698 · doi:10.1038/s41423-026-01395-x
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Also filed as BioProject PRJNA1217043 and SRA study SRP560640. Searching any of these in the dataset finder brings you back here.

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