ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Orosomucoid 1 Ameliorates Temporomandibular Joint Osteoarthritis by Maintaining Cartilage Homeostasis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Recombinant IL-38 Alleviates Temporomandibular Joint Synovial Inflammation via IL-1R1-NF-κB-IL1β Pathway.International dental journal · 2026Article
- NsPEFs-enriched ADSCs-EVs alleviate osteoarthritis via RSPO3-mediated dual pro-chondrogenic and pro-M2 macrophage properties.Bioactive materials · 2026Article
- Photothermal reprogramming of synovial M1 macrophages reshapes the pro-inflammatory microenvironment to reverse temporomandibular joint osteoarthritis.Journal of nanobiotechnology · 2026Article
- Intelligent GelMA microspheres co-loaded with BMSCs and Kartogenin for spatiotemporally controlled release and immunomodulatory regeneration of temporomandibular joint osteoarthritis.Frontiers in immunology · 2026Article
- Targeting subchondral osteoporosis in osteoarthritis: biomechanical crosstalk and the therapeutic rationale for inflammatory microenvironment remodeling.Frontiers in immunology · 2026Review
- Article
- Orosomucoid 1 Ameliorates Temporomandibular Joint Osteoarthritis by Maintaining Cartilage Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Temporomandibular joint osteoarthritis (TMJOA) is one of the most complex temporomandibular disorders. Cartilage matrix degradation results in the infiltration of nerves, blood vessels, and inflammatory cells, which disrupts chondrocyte function. Therapeutic strategies for TMJOA designed to maintain cartilage homeostasis remain largely unknown. Here, it is reported that orosomucoid 1 (ORM1) attenuated TMJOA progression by maintaining cartilage homeostasis. It is demonstrated that ORM1 is down-regulated in the synovial fluid of patients with TMJOA and condylar cartilage of unilateral anterior crossbite (UAC) rats. Administration of ORM1 protein significantly inhibited cartilage matrix degradation and alleviated TMJOA progression in UAC rats. At the mechanistic level, ORM1 binds to vimentin (VIM), a type III intermediate filament cytoskeletal protein, and inhibits the mitogen-activated protein kinase (MAPK) pathway, thereby significantly decreasing cartilage matrix degradation mediated through inhibiting the cartilage degradation markers matrix metalloproteinase 13 (MMP13) and MMP3, and maintaining cartilage homeostasis. Notably, inhibition of VIM in vivo also markedly improved TMJOA progression, including cartilage degradation and subchondral bone destruction. In conclusion, these findings demonstrate the important functions of ORM1 in maintaining cartilage homeostasis via suppressing VIM/MAPK/MMP signaling and suggest that ORM1 is a promising target for therapeutic intervention in TMJOA.
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