ArticleJournal of orthopaedic translation2020
Defactinib attenuates osteoarthritis by inhibiting positive feedback loop between H-type vessels and MSCs in subchondral bone.
Article in Journal of orthopaedic translation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Cell communication and relevant signaling pathways in osteogenesis-angiogenesis coupling.Bone research · 2025Review
- [Pathology of Cartilage-to-Bone Crosstalk: A New Angle for Animal Experimental Studies on Osteoarthritis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Review
- Targeting type H vessels with bioactive metabolites from traditional Chinese botanical drugs: a therapeutic strategy for skeletal disorders.Frontiers in pharmacology · 2025Review
- Sensory nerve EP4 facilitates heterotopic ossification by regulating angiogenesis-coupled bone formation.Journal of orthopaedic translation · 2024Article
- Targeting type H vessels in bone-related diseases.Journal of cellular and molecular medicine · 2024Review
- HIF-1Biomaterials translational · 2024Article
- Maintaining hypoxia environment of subchondral bone alleviates osteoarthritis progression.Science advances · 2023Article
- Endothelial PDGF-BB/PDGFR-β signaling promotes osteoarthritis by enhancing angiogenesis-dependent abnormal subchondral bone formation.Bone research · 2022Article
- Tropoelastin improves adhesion and migration of intra-articular injected infrapatellar fat pad MSCs and reduces osteoarthritis progression.Bioactive materials · 2022Article
- Bibliometric insights from publications on subchondral bone research in osteoarthritis.Frontiers in physiology · 2022Article
- miRNA-Gene Interaction Network Construction Strategy to Discern Promising Traditional Chinese Medicine against Osteoporosis.BioMed research international · 2022Article
- Aucubin Impeded Preosteoclast Fusion and Enhanced CD31Stem cells international · 2022Article
- Brown Adipose Tissue Rescues Bone Loss Induced by Cold Exposure.Frontiers in endocrinology · 2021Article
- Innovative designs and procedures for fracture fixation and soft tissue repair.Journal of orthopaedic translation · 2020Article
- Subchondral Bone Remodeling: A Therapeutic Target for Osteoarthritis.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAbnormal bone formation in subchondral bone resulting from uncoupled bone remodeling is considered a central feature in osteoarthritis (OA) pathogenesis. H-type vessels can couple angiogenesis and osteogenesis. We previously revealed that elevated H-type vessels in subchondral bone were correlated with OA and focal adhesion kinase (FAK) in MSCs is critical for H-type vessel formation in osteoporosis. The aim of this study was to explore the correlation between H-type vessels and MSCs in OA pathogenesis through regulation of H-type vessel formation using defactinib (an FAK inhibitor).
methods
resultsThis study demonstrated that inhibition of H-type vessels with defactinib alleviated OA by inhibiting H-type vessel-linked MSCs in subchondral bone. During OA pathogenesis, H-type vessels and MSCs formed a positive feedback loop contributing to abnormal bone formation in subchondral bone. Elevated H-type vessels provided indispensable MSCs for abnormal bone formation in subchondral bone. Flow cytometry and immunostaining results confirmed that the amount of MSCs in subchondral bone was obviously higher in vehicle-treated ACLT mice than that in sham controls and defactinib-treated ACLT mice.
conclusionsOur results demonstrate that defactinib inhibits OA by suppressing the positive feedback loop between H-type vessels and MSCs in subchondral bone. THE TRANSLATIONAL POTENTIAL OF THIS ARTICLE: Our results provide a mechanistic rationale for the use of defactinib as an effective candidate for OA treatment.
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