Chronic Inflammation and Aging in Rheumatic Diseases

Cellular senescence and immunosenescence drive chronic tissue damage via persistent senescence-associated secretory phenotype (SASP)-mediated inflammation, particularly through pro-inflammatory cytokines, including interleukin-6 (IL-6), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α). In osteoarthritis (OA), senescent chondrocytes promote cartilage degradation, while in rheumatoid arthritis (RA), aged immune cells impair self-tolerance. Emerging therapies targeting these mechanisms - including senolytics and cytokine inhibitors-demonstrate potential to break this pathological cycle. These findings emphasize the necessity of combined anti-inflammatory and anti-aging approaches for managing age-related rheumatic diseases.