Involvement of the Wnt/β‐catenin signalling pathway in heterotopic ossification and ossification‐related diseases

• Published in: Journal of cellular and molecular medicine Vol. 28; no. 18; pp. e70113 - n/a
• Main Authors: Zhao, Yike, Liu, Fangzhou, Pei, Yiran, Lian, Fengyu, Lin, Hui
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01.09.2024; John Wiley and Sons Inc
• Subjects: Angiogenesis; Animals; beta Catenin - metabolism; Bone growth; Bones; Cartilage; Catenin; Cell Differentiation; Chondrocytes; Chondrogenesis; Fibroblasts; Hedgehog protein; heterotopic ossification; Humans; Hypertrophy; Inflammation; Ligaments; MicroRNAs - genetics; MicroRNAs - metabolism; Mineralization; molecular mechanism; Ossification (ectopic); Ossification, Heterotopic - genetics; Ossification, Heterotopic - metabolism; Ossification, Heterotopic - pathology; Osteoblastogenesis; Osteoblasts - metabolism; Osteoblasts - pathology; Osteogenesis; Osteogenesis - genetics; Patients; Physiology; Review; Signal transduction; Soft tissues; Stem cells; therapeutic measures; Trauma; Wnt protein; Wnt Signaling Pathway; Wnt/β‐catenin signalling; heterotopic ossification; molecular mechanism; therapeutic measures; Wnt/β‐catenin signalling
• ISSN: 1582-1838; 1582-4934; 1582-4934
• DOI: 10.1111/jcmm.70113

Heterotopic ossification (HO) is a pathological condition characterized by the formation of bone within soft tissues. The development of HO is a result of abnormal activation of the bone formation programs, where multiple signalling pathways, including Wnt/β‐catenin, BMP and hedgehog signalling, are involved. The Wnt/β‐catenin signalling pathway, a conserved pathway essential for various fundamental activities, has been found to play a significant role in pathological bone formation processes. It regulates angiogenesis, chondrocyte hypertrophy and osteoblast differentiation during the development of HO. More importantly, the crosstalk between Wnt signalling and other factors including BMP, Hedgehog signalling, YAP may contribute in a HO‐favourable manner. Moreover, several miRNAs may also be involved in HO formation via the regulation of Wnt signalling. This review aims to summarize the role of Wnt/β‐catenin signalling in the pathogenesis of HO, its interactions with related molecules, and potential preventive and therapeutic measures targeting Wnt/β‐catenin signalling.