Figure 3.

Role of OPN in cardiovascular system aging. The cytokine interleukin (IL)-18 and aging are involved in inducing OPN expression and promoting myocardial fibrosis and cardiac dysfunction. when OPN-/-, the adhesion of cardiac fibroblasts to extracellular matrices (ECM) is greatly reduced, the expression level of miR-21 decreases and β1AR and β₂AR are activated to enhance the production of cAMP, increasing the protein level of Epac1 to combat the fibrosis of cardiac fibroblasts. Whereas an injection of the recombinant OPN protein reactivates the AP1/miR-21/PTEN and SMAD7 pathways and enhances fibrosis. OPN has two sides to vascular calcification, on the one hand, OPN activated the MAPK signaling pathway, and the imbalance of Akt and MAPK pathways leads to the switching of vascular smooth muscle cells (VSMCs) to pathological progression. on the other hand, OPN is an effective physiological inhibitor of endogenous mineralization, which can prevent ectopic calcium deposition, and is an effective inhibitor of vascular calcification.