ArticleNature communications2026
Cartilage targeting hydrogel nanoplatform degrades BRD4 to alleviate osteoarthritis via Nav1.7 axis.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- A biomimetic chondrocyte membrane-camouflaged tFNA nanoplatform for reprogramming the cartilage-synovium axis in osteoarthritis.Materials today. Bio · 2026Article
- Delivering Degradation: Nanomedicine and Programmable Proximity Platforms for Targeted Protein Degradation.Pharmaceutics · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a common degenerative joint disease with limited disease-modifying therapies. Emerging evidence suggests that epigenetic dysregulation contributes to cartilage degeneration, but effective strategies to selectively target these pathways remain lacking. Here we show that the BRD4/Nav1.7 axis drives inflammatory and metabolic dysfunction in OA. Integrated single-cell and transcriptomic analyses identify BRD4 as a key regulator that enhances Nav1.7 transcription, promoting mitochondrial impairment and catabolic activation in chondrocytes. To therapeutically target this pathway, we develop a biomimetic hydrogel system incorporating chondrocyte membrane-coated nanoparticles for cartilage-specific delivery of a BRD4 proteolysis-targeting chimera (PROTAC), a molecule designed to induce selective protein degradation. This nanoplatform enables efficient intra-articular delivery, immune evasion and targeted retention in cartilage. Treatment suppresses inflammatory responses, restores mitochondrial function and reduces cartilage degeneration and pain behaviors in two mouse models of OA. These findings establish targeted BRD4 degradation as a disease-modifying strategy and provide a precision nanotherapeutic platform for OA.
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Registered trials
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