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Cited by 331

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Modulation of bone morphogenetic protein signaling inhibits the onset and progression of ankylosing enthesitis

Open access
Lories, Rik J.U., Derese, Inge, Luyten, Frank P.·2005·Journal of Clinical Investigation

Abstract

Joint ankylosis is a major cause of disability in the human spondyloarthropathies. Here we report that this process partially recapitulates embryonic endochondral bone formation in a spontaneous model of arthritis in DBA/1 mice. Bone morphogenetic protein (BMP) signaling appears to be a key molecular pathway involved in this pathological cascade. Systemic gene transfer of noggin, a BMP antagonist, is effective both as a preventive and a therapeutic strategy in the mouse model, mechanistically interfering with enthesial progenitor cell proliferation in early stages of the disease process. Immunohistochemical staining for phosphorylated smad1/5 in enthesial biopsies of patients with spondyloarthropathy reveals active BMP signaling in similar target cells. Our data suggest that BMP signaling is an attractive therapeutic target for interfering with structural changes in spondyloarthropathy either as an alternative or complementary approach to current antiinflammatory treatments.

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Metadata

Authors
Lories, R. J. U., Derese, I., & Luyten, F. P.
Venue
Journal of Clinical Investigation
Published
2005-06-01
Volume
115
Issue
6
Pages
1571-1579
ISSN
0021-9738 (ISSN-L)
OpenAlex
W1984088097
Cited by
331
References
1
FWCI
8.83
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Modulation of bone morphogenetic protein signaling inhibits the onset and progression of ankylosing enthesitis. https://app.cochat.ai/papers/10.1172/jci23738
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Lories, R. J. U., Derese, I., & Luyten, F. P. (2005). Modulation of bone morphogenetic protein signaling inhibits the onset and progression of ankylosing enthesitis. Journal of Clinical Investigation. https://doi.org/10.1172/jci23738

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.