ArticleOsteoarthritis and cartilage2023
CAMKK2 is upregulated in primary human osteoarthritis and its inhibition protects against chondrocyte apoptosis.
Article in Osteoarthritis and cartilage, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Thread- reinforced encapsulation devices (THRED) for therapeutic stem cell delivery.Journal of pediatric surgery · 2026Article
- Blocking calcium-MYC regulatory axis inhibits early dedifferentiation of chondrocytes and contributes to cartilage regeneration.Stem cell research & therapy · 2025Article
- Integrated plasma and vegetation proteomic characterization of infective endocarditis for early diagnosis and treatment.Nature communications · 2025Article
- Exosomes-Shuttled lncRNA SNHG7 by Bone Marrow Mesenchymal Stem Cells Alleviates Osteoarthritis Through Targeting miR-485-5p/FSP1 Axis-Mediated Chondrocytes Ferroptosis and Inflammation.Tissue engineering and regenerative medicine · 2024Article
- CHMP5 attenuates osteoarthritis via inhibiting chondrocyte apoptosis and extracellular matrix degradation: involvement of NF-κB pathway.Molecular medicine (Cambridge, Mass.) · 2024Article
- A Reproducible Cartilage Impact Model to Generate Post-Traumatic Osteoarthritis in the Rabbit.Journal of visualized experiments : JoVE · 2023Article
- Inflammatory mechanisms in post-traumatic osteoarthritis: a role for CaMKK2.Immunometabolism (Cobham, Surrey) · 2023Review
- Identification of EGFR as an essential regulator in chondrocytes ferroptosis of osteoarthritis using bioinformatics,Heliyon · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
objectiveTo investigate the role of calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) in human osteoarthritis. MATERIALS AND
methodsPaired osteochondral plugs and articular chondrocytes were isolated from the relatively healthier (intact) and damaged portions of human femoral heads collected from patients undergoing total hip arthroplasty for primary osteoarthritis (OA). Cartilage from femoral plugs were either flash frozen for gene expression analysis or histology and immunohistochemistry. Chondrocyte apoptosis in the presence or absence of CAMKK2 inhibition was measured using flow cytometry. CAMKK2 overexpression and knockdown in articular chondrocytes were achieved via Lentivirus- and siRNA-mediated approaches respectively, and their effect on pro-apoptotic and cartilage catabolic mechanisms was assessed by immunoblotting.
resultsCAMKK2 mRNA and protein levels were elevated in articular chondrocytes from human OA cartilage compared to paired healthier intact samples. This increase was associated with elevated catabolic marker matrix metalloproteinase 13 (MMP-13), and diminished anabolic markers aggrecan (ACAN) and type II collagen (COL2A1) levels. OA chondrocytes displayed enhanced apoptosis, which was suppressed following pharmacological inhibition of CAMKK2. Levels of MMP13, pSTAT3, and the pro-apoptotic marker BAX became elevated when CAMKK2, but not its kinase-defective mutant was overexpressed, whereas knockdown of the kinase decreased the levels of these proteins.
conclusionsCAMKK2 is upregulated in human OA cartilage and is associated with elevated levels of pro-apoptotic and catabolic proteins. Inhibition or knockdown of CAMKK2 led to decreased chondrocyte apoptosis and catabolic protein levels, whereas its overexpression elevated them. CAMKK2 may be a therapeutic target to prevent or mitigate human OA.
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