GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE288nnn/GSE288373/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE288373GEOGSEfalseTofacitinib Repairs GM-CSF-induced RA Mitochondrial DysfunctionRheumatoid 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.2026/04/08GSE288373GSM8766510GSM8766505GSM8766506GSM8766509GSM8766507GSM87665083428424676288373Homo sapiens[41781698]