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Wnt Pathway in Bone Repair and Regeneration - What Do We Know So Far

Authors
 Khosrow S Houschyar  ;  Christian Tapking  ;  Mimi R Borrelli  ;  Daniel Popp  ;  Dominik Duscher  ;  Zeshaan N Maan  ;  Malcolm P Chelliah  ;  Jingtao Li  ;  Kamran Harati  ;  Christoph Wallner  ;  Susanne Rein  ;  Dominik Pförringer  ;  Georg Reumuth  ;  Gerrit Grieb  ;  Sylvain Mouraret  ;  Mehran Dadras  ;  Johannes M Wagner  ;  Jungul Y Cha  ;  Frank Siemers  ;  Marcus Lehnhardt  ;  Björn Behr 
Citation
 FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY, Vol.6 : 170, 2019-01 
Journal Title
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
Issue Date
2019-01
Keywords
Wnt ; bone ; canonical ; non-canonical ; regeneration ; repair ; stem cells ; β-catenin
Abstract
Wnt signaling plays a central regulatory role across a remarkably diverse range of functions during embryonic development, including those involved in the formation of bone and cartilage. Wnt signaling continues to play a critical role in adult osteogenic differentiation of mesenchymal stem cells. Disruptions in this highly-conserved and complex system leads to various pathological conditions, including impaired bone healing, autoimmune diseases and malignant degeneration. For reconstructive surgeons, critically sized skeletal defects represent a major challenge. These are frequently associated with significant morbidity in both the recipient and donor sites. The Wnt pathway is an attractive therapeutic target with the potential to directly modulate stem cells responsible for skeletal tissue regeneration and promote bone growth, suggesting that Wnt factors could be used to promote bone healing after trauma. This review summarizes our current understanding of the essential role of the Wnt pathway in bone regeneration and repair.
Files in This Item:
T999201859.pdf Download
DOI
10.3389/fcell.2018.00170
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Orthodontics (교정과학교실) > 1. Journal Papers
Yonsei Authors
Cha, Jung Yul(차정열)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/188914
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