English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

Although osteoarthritis (OA) in the hip joint is a common and debilitating degenerative disease, the precise molecular mechanisms underlying its pathological process remains unclear. This study sets out to investigate whether β‐catenin plays a critical role in hip OA pathogenesis. Here, we showed overexpressed β‐catenin protein in human OA cartilage tissues. Then, we analyzed  β‐cat(ex3)   Col2ER   mice, in which  β‐catenin  gene was conditionally activated in femoral head chondrocytes. At 2 months of age,  β‐cat(ex3)   Col2ER   mice already showed a phenotype of severe cartilage degeneration in the femoral head. More changes observed in  β‐cat(ex3)   Col2ER   mice with age included subchondral sclerosis and osteophyte formation along joint margins, resembling a hip OA phenotype in humans. In addition, cartilage degradation and chondrocyte apoptosis as the results of  β‐catenin  activation possibly contributed to this hip OA‐like phenotype. Overall our findings provide direct evidence about the importance of β‐catenin in hip OA pathogenesis.

Activation of β‐catenin in Col2 ‐expressing chondrocytes leads to osteoarthritis‐like defects in hip joint