ArticleInternational journal of oral science2022
Kindlin-2 loss in condylar chondrocytes causes spontaneous osteoarthritic lesions in the temporomandibular joint in mice.
Article in International journal of oral science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 29 citations in OpenAlex.
- Sustained Hypoxia-Inducible Factor 1-Alpha Accumulation Disrupts the Articular Niche to Promote Osteoarthritis Pathogenesis.Aging cell · 2026Article
- Nasal Chondrocytes Intensively Invade and Repair Pathologically Altered Cartilage Through Intrinsic Genomic Mechanisms: A Narrative Review.Current rheumatology reviews · 2026Review
- Nano MiRNA-Functionating Tetrahedral Framework Nucleic Acid for Cartilage-Targeted Ferritinophagy Modulation to Attenuate Temporomandibular Joint Osteoarthritis.Small science · 2026Article
- Article
- Osteocytic vinculin controls bone mass by modulating Mef2c-driven sclerostin expression in mice.Bone research · 2025Article
- Targeting Piezo1 channel to alleviate intervertebral disc degeneration.Journal of orthopaedic translation · 2025Article
- A loss of primary cilia by a reduction in mTOR signaling correlates with age-related deteriorations in condylar cartilage.GeroScience · 2024Article
- Pip5k1γ promotes anabolism of nucleus pulposus cells and intervertebral disc homeostasis by activating CaMKII-Ampk pathway in aged mice.Aging cell · 2024Article
- Targeting miR-29 mitigates skeletal senescence and bolsters therapeutic potential of mesenchymal stromal cells.Cell reports. Medicine · 2024Article
- Multi-class segmentation of temporomandibular joint using ensemble deep learning.Scientific reports · 2024Article
- Piezo1 activation accelerates osteoarthritis progression and the targeted therapy effect of artemisinin.Journal of advanced research · 2024Article
- Integrin signalling in joint development, homeostasis and osteoarthritis.Nature reviews. Rheumatology · 2024Review
- Gentiopicroside ameliorates the lipopolysaccharide-induced inflammatory response and hypertrophy in chondrocytes.Journal of orthopaedic surgery and research · 2024Article
- FLRT2 mediates chondrogenesis of nasal septal cartilage and mandibular condyle cartilage.Open medicine (Warsaw, Poland) · 2024Article
- Resatorvid alleviates experimental inflammatory TMJOA by restraining chondrocyte pyroptosis and synovial inflammation.Arthritis research & therapy · 2023Article
- Loss of Pinch Proteins Causes Severe Degenerative Disc Disease-Like Lesions in Mice.Aging and disease · 2023Article
- Comparison of Kindlin-2 deficiency-stimulated osteoarthritis-like lesions induced byJournal of orthopaedic translation · 2023Article
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Brief research report: Effects of Pinch deficiency on cartilage homeostasis in adult mice.Frontiers in cell and developmental biology · 2023Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint (TMJ) osteoarthritis (OA); however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhesion protein, is strongly detected in cells of mandibular condylar cartilage in mice. We find that genetic ablation of Kindlin-2 in aggrecan-expressing condylar chondrocytes induces multiple spontaneous osteoarthritic lesions, including progressive cartilage loss and deformation, surface fissures, and ectopic cartilage and bone formation in TMJ. Kindlin-2 loss significantly downregulates the expression of aggrecan, Col2a1 and Proteoglycan 4 (Prg4), all anabolic extracellular matrix proteins, and promotes catabolic metabolism in TMJ cartilage by inducing expression of Runx2 and Mmp13 in condylar chondrocytes. Kindlin-2 loss decreases TMJ chondrocyte proliferation in condylar cartilages. Furthermore, Kindlin-2 loss promotes the release of cytochrome c as well as caspase 3 activation, and accelerates chondrocyte apoptosis in vitro and TMJ. Collectively, these findings reveal a crucial role of Kindlin-2 in condylar chondrocytes to maintain TMJ homeostasis.
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