Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by inflammatory cell infiltration, high levels of cytokines, and erosion of cartilage and bone in joints. Calprotectin (CLP), as a recently described member of S100 family proteins, is a heterodimeric complex of S100A8 and S100A9. Currently, plenty of studies have indicated significantly increased serum and synovial fluid levels of CLP in patients with RA. It was reported that CLP was related to cell differentiation, migration, apoptosis, and production of pro-inflammatory factors in RA. In addition, there are the positive relationships between serum, synovial CLP and traditional acute phase reactants, disease activity, ultrasound and radiographic progression of joints, and treatment response of RA. In this review, we mainly discuss the role of CLP in the pathogenesis of RA as well as its potential to estimate clinical disease progression of RA patients.
Rheumatoid arthritis (RA) is a chronic autoimmune disease and is supposed to have both genetic and environmental backgrounds. Plenty of studies have demonstrated the roles of long non-coding RNAs (lncRNAs) in the initiation and development of RA. Numerous lncRNAs have been found to be dysregulated in RA and to be correlated with disease activity of RA, which indicates potential diagnostic roles of lncRNAs. In addition to working as biomarkers for RA, lncRNAs participate in many specific pathological processes including inflammation, aberrant proliferation, migration, invasion and apoptosis. Further screenings and researches are required to validate the clinical potentials of lncRNAs as diagnostic and therapeutic targets in RA.