Authors
Chunlu Yan, Chuangwei Sui, Qiao Wan, Xupeng Liu, Zeling Fang, Jiarong Shi, Chen Chen, Yu Jiang, Juan Yu, Fangyu An
Published in
Cells. Volume 15. Issue 14. Jul 22, 2026. Epub Jul 22, 2026.
Abstract
The pathogenesis of knee osteoarthritis (KOA) involves bone homeostasis imbalance induced by inflammation, metabolism, age, mechanical stress, joint injury and other factors. Recently, Type H vessels (CD31hiEMCNhi endothelial cells) have emerged as a specialized endothelial cell subset that couples angiogenesis with osteogenesis. Type H angiogenesis in the diaphysis was found to be beneficial for maintaining bone homeostasis, while the abnormal proliferation of type H vessels in subchondral bone can lead to chondrocyte hypertrophy and osteophyte formation. However, the mechanism by which the abnormal proliferation of type H vessels induces KOA has not been elucidated in detail. In this review, we summarize the latest evidence on the role of type H endothelial cell function in the pathogenesis and progression of osteoarthritis (OA). We review the role of type H angiogenesis at different sites in the development and progression of OA and focus on the potential mechanisms that regulate type H angiogenesis in OA and the potential therapeutic value and significance of targeting type H angiogenesis in promoting bone regeneration and maintaining bone homeostasis. Finally, we discuss key obstacles and future directions for studying type H vessel regulation in KOA, offering an endothelial cell-based framework for understanding bone homeostasis and improving OA.
PMID:
42505419
Bibliographic data and abstract were imported from PubMed on 14 Sep 2026.
Read full publication at:
Please sign in
to see all details.
Advertisement
Stats
- Recommendations n/a n/a positive of 0 vote(s)
- Views 4
- Comments 0