Academic Bibliography

 Search 200 years of publications by Ghent University researchers.
Advanced search
1 file | 13.56 MB
Add to list
  1. Search results
  2. GDF15 mediates inflammation-associate...

GDF15 mediates inflammation-associated bone loss through a brain-bone axis

Renée Van der Cruyssen (UGent) , Jan Devan, Irina Heggli, Dominik Burri, Djoere Gaublomme (UGent) , Iván Josipovic (UGent) , Emilie Dumas (UGent) , Carolien Vlieghe (UGent) , Maria Gabriella Raimondo, Pavel Zakharov, et al.
(2023) BIORXIV.
Author
Organization
Abstract
Metabolic mediators play an important role in regulating chronic inflammation in the body. Here we report an unexpected role for GDF15 (Growth Differentiation Factor 15), a central mediator of food intake, in inflammation-associated bone loss. GDF15 serum levels were found to be elevated in arthritis patients and inversely correlated with bone density. Despite being associated with inflammation, we found that GDF15 itself does not cause, nor contribute to, clinical or histopathological arthritis. Rather, under inflammatory conditions, GDF15 mediates trabecular bone loss through its receptor GFRAL, which is exclusively expressed in the hindbrain. GDF15-GFRAL binding results in β-adrenergic activation of MALPs (Marrow Adipocytic Lineage Precursors) in the bone marrow, which stimulate osteoclasts and trigger bone loss. These data suggest a metabolic mediator-controlled brain-bone axis in inflammation, through which bone loss is induced in a contextual rather than general manner. These findings may lead to more specific therapeutic interventions to protect bone.

Downloads

  • Download
    2023 Renee Elewaut GDF15 preprint 2023.11.22.568290v1.full.pdf
    • full text (Author's original)
    • |
    • open access
    • |
    • PDF
    • |
    • 13.56 MB

Citation

Please use this url to cite or link to this publication:

MLA
Van der Cruyssen, Renée, et al. “GDF15 Mediates Inflammation-Associated Bone Loss through a Brain-Bone Axis.” BIORXIV, 2023, doi:10.1101/2023.11.22.568290.
APA
Van der Cruyssen, R., Devan, J., Heggli, I., Burri, D., Gaublomme, D., Josipovic, I., … Elewaut, D. (2023). GDF15 mediates inflammation-associated bone loss through a brain-bone axis. https://doi.org/10.1101/2023.11.22.568290
Chicago author-date
Van der Cruyssen, Renée, Jan Devan, Irina Heggli, Dominik Burri, Djoere Gaublomme, Iván Josipovic, Emilie Dumas, et al. 2023. “GDF15 Mediates Inflammation-Associated Bone Loss through a Brain-Bone Axis.” BIORXIV. https://doi.org/10.1101/2023.11.22.568290.
Chicago author-date (all authors)
Van der Cruyssen, Renée, Jan Devan, Irina Heggli, Dominik Burri, Djoere Gaublomme, Iván Josipovic, Emilie Dumas, Carolien Vlieghe, Maria Gabriella Raimondo, Pavel Zakharov, Peggy Jacques, Sophie De Mits, Zuzanna Łukasik, Marnik Vuylsteke, Thomas Renson, Lisa Schots, Guillaume Planckaert, Flore Stappers, Tine Decruy, Julie Coudenys, Teddy Manuello, Lars Vereecke, Ruslan Dmitriev, Stijn Lambrecht, Luc Van Hoorebeke, Jo Lambert, Kodi Ravichandran, Andreas Ramming, Stefan Dudli, Georg Schett, Eric Gracey, and Dirk Elewaut. 2023. “GDF15 Mediates Inflammation-Associated Bone Loss through a Brain-Bone Axis.” BIORXIV. doi:10.1101/2023.11.22.568290.
Vancouver
1.
Van der Cruyssen R, Devan J, Heggli I, Burri D, Gaublomme D, Josipovic I, et al. GDF15 mediates inflammation-associated bone loss through a brain-bone axis. BIORXIV. 2023.
IEEE
[1]
R. Van der Cruyssen et al., “GDF15 mediates inflammation-associated bone loss through a brain-bone axis,” BIORXIV. 2023.
@misc{01HJ13XN44H67HG2MTSSWMDNC7,
  abstract     = {{Metabolic mediators play an important role in regulating chronic inflammation in the body. Here we report an unexpected role for GDF15 (Growth Differentiation Factor 15), a central mediator of food intake, in inflammation-associated bone loss. GDF15 serum levels were found to be elevated in arthritis patients and inversely correlated with bone density. Despite being associated with inflammation, we found that GDF15 itself does not cause, nor contribute to, clinical or histopathological arthritis. Rather, under inflammatory conditions, GDF15 mediates trabecular bone loss through its receptor GFRAL, which is exclusively expressed in the hindbrain. GDF15-GFRAL binding results in β-adrenergic activation of MALPs (Marrow Adipocytic Lineage Precursors) in the bone marrow, which stimulate osteoclasts and trigger bone loss. These data suggest a metabolic mediator-controlled brain-bone axis in inflammation, through which bone loss is induced in a contextual rather than general manner. These findings may lead to more specific therapeutic interventions to protect bone.}},
  author       = {{Van der Cruyssen, Renée and Devan, Jan and Heggli, Irina and Burri, Dominik and Gaublomme, Djoere and Josipovic, Iván and Dumas, Emilie and Vlieghe, Carolien and Raimondo, Maria Gabriella and Zakharov, Pavel and Jacques, Peggy and De Mits, Sophie and Łukasik, Zuzanna and Vuylsteke, Marnik and Renson, Thomas and Schots, Lisa and Planckaert, Guillaume and Stappers, Flore and Decruy, Tine and Coudenys, Julie and Manuello, Teddy and Vereecke, Lars and Dmitriev, Ruslan and Lambrecht, Stijn and Van Hoorebeke, Luc and Lambert, Jo and Ravichandran, Kodi and Ramming, Andreas and Dudli, Stefan and Schett, Georg and Gracey, Eric and Elewaut, Dirk}},
  language     = {{eng}},
  pages        = {{46}},
  series       = {{BIORXIV}},
  title        = {{GDF15 mediates inflammation-associated bone loss through a brain-bone axis}},
  url          = {{http://doi.org/10.1101/2023.11.22.568290}},
  year         = {{2023}},
}
Altmetric
View in Altmetric