We aimed to understand how iron affects autoimmune disorders, specifically focusing on rheumatoid arthritis (RA). Our study explored the function of ferroportin (FPN), a membrane iron transporter, in the proliferation and movement of fibroblast-like synoviocytes (FLS) linked to RA.
We found that FPN levels were significantly lower in RA tissues compared to normal tissues, hinting at a potential connection between iron metabolism and the disease. By conducting a series of assays, we demonstrated that increased FPN expression leads to a slowdown in FLS growth and migration. This effect seems to be mediated through the suppression of the PI3K/AKT signaling pathway and is accompanied by elevated levels of reactive oxygen species (ROS).
These findings suggest that ferroportin might play a crucial role in the development of RA by regulating iron levels in FLS. This insight opens new avenues for potential treatments targeting iron dysregulation to help alleviate joint damage in RA patients.