Medical devices implanted in the body for drug delivery, sensing, or tissue regeneration usually come under fire from the host’s immune system. Defense cells work to isolate material they consider foreign to the body, building up a wall of dense scar tissue around the devices, which eventually become unable to perform their functions.
Researchers at MIT and Boston Children’s Hospital have identified a signaling molecule that is key to this process of “fibrosis,” and they have shown that blocking the molecule prevents the scar tissue from forming. The findings, reported in the Nature Materials, could help scientists extend the lifespan of many types of implantable medical devices.
