Synovitis and gradual joint degeneration are hallmarks of rheumatoid arthritis (RA), a chronic inflammatory illness. To sustain inflammation and tissue damage, pathogenic immune and stromal cells undergo specific metabolic reprogramming that alters glycolysis, oxidative phosphorylation, and lipid metabolism. This pathology is driven by immunometabolic dysregulation, according to new research. This review summarizes the current understanding of cell-type-specific immunometabolic dysregulation in RA, with particular attention to T cells, macrophages, B cells, and fibroblast-like synoviocytes. We assess how high-dimensional biomarkers, such as blood-based metabolomic, transcriptomic, and proteomic signatures, and synovial molecular pathotypes can be used to stratify patients and predict how well biologic and targeted treatments will work. We also reviewed treatment approaches targeting immunometabolic pathways, including new metabolic inhibitors and drug repurposing, such as metformin. To facilitate a more individualized and efficient RA treatment, we conclude by offering a clinically applicable paradigm to integrate immunometabolic profiling into precision medicine.
Liu et al. (2026) studied this question.