Abstract Immunometabolic dysregulation has emerged as a key driver in the pathogenesis of autoimmune rheumatic diseases (ARDs), including rheumatoid arthritis (RA), osteoarthritis (OA), and systemic lupus erythematosus (SLE). This review highlighted the central role of glycolytic reprogramming in driving immune cell dysfunction and disease progression. In RA, enhanced glycolysis promoted T cell dysregulation, synovial fibroblast activation, and macrophage polarization.