ArticleNature aging2022
Kindlin-2 preserves integrity of the articular cartilage to protect against osteoarthritis.
Article in Nature aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 83 citations in OpenAlex.
- Dual regulation of inflammation and ferroptosis: An injectable hydrogel targeting macrophages for the treatment of temporomandibular joint osteoarthritis and knee osteoarthritis.Materials today. Bio · 2026Article
- The inhibition of lactate/Gpr81 signalling driven by moderate-intensity continuous training protects against osteoarthritis.Experimental & molecular medicine · 2026Article
- Purinergic signaling in osteoarthritis: Mechanistic insights into pathogenesis and therapeutic targeting.Genes & diseases · 2026Review
- Multi-Technique Integration Identifies O-GlcNAc Transferase in Fibroblast-Like Synoviocytes as a Therapeutic Target for Rheumatoid Arthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Adipose-derived mesenchymal stem cell injection into the KI10 acupoint mitigates cartilage damage in KOA rats through PGE2-mediated α7nAChR/NF-κB pathway.Animal models and experimental medicine · 2026Article
- In Situ Profiling of Nanoscale Strains Uncovers Mechano-Architectural Predictors of Aging and Osteoarthritis Emergence.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Epigenetic modulation of the JAK2-STAT3 signaling pathway in osteoporosis: non-coding RNA networks as therapeutic targets.Journal of translational medicine · 2026Review
- Sustained Hypoxia-Inducible Factor 1-Alpha Accumulation Disrupts the Articular Niche to Promote Osteoarthritis Pathogenesis.Aging cell · 2026Article
- DCLK1-dependent NF-κB activation mediates p-STAT3-induced osteoarthritis progression.Clinical and translational medicine · 2026Article
- Role of external forces in the mechanobiology of stem and differentiated chondrogenic cells embedded in a tissue-engineered construct for cartilage repair.Journal of biomedical science · 2026Review
- Mechanical Overloading-Induced Nanomineral Crystal Perturbation from the Osteochondral Interface: A Potential Initiator of Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Talin1 loss activates DRG neurons to accelerate bone remodeling and fracture healing in mice.Journal of orthopaedic translation · 2026Article
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- STOML2 Alleviates Osteoarthritis by Regulating Mitochondrial Energy Metabolism and Oxidative Stress.Genetics research · 2026Article
- IFT88/Kindlin-2 Signaling Prevents Mechanical Overloading-Induced PANoptosis of Nucleus Pulposus Cells by Activating FOXP1 SUMOylation.International journal of biological sciences · 2026Article
- Enhancement of antibiotic therapy in osteomyelitis by inhibiting talin-1-mediated bacterial internalization.Frontiers in cellular and infection microbiology · 2026Article
- The Sirt1-Piezo1 Axis Promotes Bone Formation and Repair in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Fexofenadine protects against osteoarthritis by targeting Smad2 and STAT1 to enhance anabolism and binding cPLA2 to inhibit catabolism.Cell death discovery · 2025Article
- Circular RNA-based protein replacement therapy mitigates osteoarthritis in male mice.Nature communications · 2025Article
- The impact of mitochondrial dysfunction on osteoarthritis cartilage: current insights and emerging mitochondria-targeted therapies.Bone research · 2025Review
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 2 countries.
Funding
Abstract
Osteoarthritis (OA) is an aging-related degenerative joint disease with a poorly defined mechanism. Here we report that kindlin-2 is highly expressed in articular chondrocytes and downregulated in the degenerated cartilage of aged mice and patients with OA. Kindlin-2 deletion in articular chondrocytes leads to spontaneous OA and exacerbates instability-induced OA lesions in adult mice. Kindlin-2 deficiency promotes mitochondrial oxidative stress and activates Stat3, leading to Runx2-mediated chondrocyte catabolism. Pharmacological inhibition of Stat3 activation or genetic ablation of Stat3 in chondrocytes reverses aberrant accumulation of Runx2 and extracellular-matrix-degrading enzymes and limits OA deteriorations caused by kindlin-2 deficiency. Deleting Runx2 in chondrocytes reverses structural changes and OA lesions caused by kindlin-2 deletion without downregulating p-Stat3. Intra-articular injection of AAV5-kindlin-2 decelerates progression of aging- and instability-induced knee joint OA in mice. Collectively, we identify a pathway consisting of kindlin-2, Stat3 and Runx2 in articular chondrocytes that is responsible for maintaining articular cartilage integrity and define a potential therapeutic target for OA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.