Fig. 1

Schematic diagram of miRNAs in normal development, homeostasis and RA progression. a In normal synovial joints, many cell types serve as major sources of short noncoding RNAs, including miRNAs, which are transcribed from DNA. Precursor miRNAs are cleaved and processed into miRNAs, which further function within parental cells and neighboring functional cells and can be secreted into biological fluids such as blood and joint fluid as free molecules or extracellular vesicles. b In normal conditions in synovial joints, miRNAs are mainly produced by a variety of cells involved in the composition of bone remodeling, osteoimmunology and synovial systems. MiRNAs procedurally regulate well-organized bone remodeling, appropriate levels of immune responses and the secretion of normal synovial fluid. Conversely, persistent synovial hyperplasia, progressive inflammation, and subsequent destruction of affected joints are prominent characteristics of RA. The development, differentiation and homeostasis of diverse cell populations in the inflamed synovial compartment are dysregulated as a result of miRNA deregulation. Interactions between these abnormal cell types with disrupted function ultimately contribute to RA pathogenesis. miRNA microRNA, APC antigen-presenting cell, RANKL receptor activator of NF-κB ligand, FLS fibroblast-like synoviocyte, MMP matrix metalloproteinase