It's long been known that an overabundance of the immune chemical TNF alpha destroys cartilage and bone in rheumatoid arthritis patients and cuts their supply of bone-building osteoblasts. New experiments at the University of Rochester determined that TNF alpha works through the Smurf1 enzyme, which turns off two proteins that spur bone development. And that insight is likely to play a role in the development of new RA drugs.

"The significance of our study is that it identifies Smurf1 as the signaling partner through which TNF does its damage in RA-related bone loss," said Lianping Xing. The finding "enables us to begin designing small molecule drugs to shut down the action of Smurf1 and its relatives. Furthermore, since mice engineered to have less Smurf1 develop thicker bones, future drugs that shut down Smurf1 may be also useful against more common forms of osteoporosis simply by changing the dose. Of course, this is early stage work with many obstacles ahead, but is exciting nonetheless."

- check out the release [1]
- read the story [2] from HealthDay

Related Articles:
Trial set for rheumatoid arthritis cure [3]
Rheumatology: fastest growing subject of trials [4]
Scientists unveil new pathway for rheumatoid arthritis [5]