Results: DKK-1 levels increased with age and in the presence of hip fractures.
2
When compared to women, men had higher SOST levels but lower DKK-1 levels.
3
Conclusions: These findings indicate that low bone formation and expression of Dkk-1 trigger inflammatory bone loss.
4
More recent data indicate that Dkk family members may also possess functions independent of Wnt-signaling during carcinogenesis.
5
Inhibition of Dkk-1 may thus be considered as a potent strategy to protect bone from inflammatory damage.
6
RTX-mediated B cell depletion may mechanistically function via the recently established TGFβ-Dkk-1 axis in improving skin fibrosis.
7
TNF-a is a key inducer of DKK-1, which belongs to the family of proteins involved in joint remodeling.
8
However, the effect of endocrine therapies on serum DKK-1 and sclerostin levels in patients with primary breast cancer remains elusive.
9
Results: In baseline biopsies obtained from all patients with SSc but not in healthy subjects, Dkk-1 was undetectable in skin fibroblasts.
10
Conclusions: This is the first study demonstrating a link between B cell depletion and skin Dkk-1 upregulation in patients with SSc.
11
Moreover, this decreased expression of TGFβ in the skin was significantly more pronounced in the subgroup of patients with Dkk-1 upregulation.
12
Medical history was obtained, a comprehensive geriatric assessment was performed and serum levels of SOST, DKK-1 and bone formation markers were analysed.
13
The costs were 83.75 DKK per scan.
14
Conclusion: DKK-1 serum levels were reduced in breast cancer patients receiving an adjuvant therapy with tamoxifen, possibly contributing to its bone-protective properties.
15
Accordingly, blocking of Dkk-1 reverses the phenotype in experimental arthritis from a pattern of bone destruction to a pattern of bone formation.
16
This was in part regulated by Dkk-1 secreted by MM cells and is a potential mechanism contributing to the osteoblast dysfunction noted in MM.