Various studies have shown that the high expression of matrix metalloproteinase-3 (MMP-3) is involved and play an important role in the degradation of the extracellular matrix of synovium, cartilage and subchondral bone of rheumatoid arthritis(RA). Tissue inhibitor of metalloproteinase 1 (TIMP-1) binds specifically to MMP-3 and inhibits the activity of MMP-3. The balance of MMP-3 / TIMP-1 plays an important role in the clinical outcome of RA. New research found that inhibiting Th17 cell differentiation, maintaining Treg (regulatory T cell) activity and regulating Th17/ Treg balance may provide novel targets for the treatment of RA. Further study found that the expression of MMP-3 and Interleukin 17(IL-17) in the peripheral blood of RA patients was significantly increased, the two were positively correlated, and the decrease of Treg could affect the balance of MMP-3/TIMP-1. This article will review the mechanism of MMP-3/TIMP-1 and Th17 /Treg in RA and its clinical significance.

Animals ; Coronary Vessels ; Diabetes Mellitus ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Rats