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Drugs, Vaccines and Therapeutics
by ruth on June 6, 2006

The researchers found that mice with enhanced NFATc activity in their osteoblasts had many more of these bone-forming cells, which explained the increase in bone mass. They also found a possible explanation for why there were more bone-destroying osteoclasts. Osteoblasts with hyperactive NFATc expressed higher levels of inflammatory proteins called chemokines, which promote osteoclast development.
According to the researchers, this findings holds a lot of promise in treating osteoporosis.
Very little NFATc1 must be activated to build extra bone, Winslow noted, which means that it may be possible to up-regulate the calcineurin/NFATc pathway to promote bone formation without disturbing other organ systems that use this same pathway.
They are now screening chemical libraries that could perform the task. Read more from the Howard Hughes Medical Institute News: A New Way to Build Bone.
[Photo: Medline Plus]
Tags:
osteoporosis
genetics
biotech
bone
target
therapeutic+target
osteoporosis+therapeutic
nfatc1+novel
Trackback: http://publish.creative-weblogging.com/publish/mt-tb.pl/23670
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