ArticleMaterials today. Bio2026
A biomimetic chondrocyte membrane-camouflaged tFNA nanoplatform for reprogramming the cartilage-synovium axis in osteoarthritis.
Article in Materials today. Bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
9 authors.
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Abstract
Osteoarthritis (OA) is a whole-joint disorder characterized by progressive cartilage degeneration and synovial remodeling, yet effective disease-modifying therapies remain unavailable. Mitochondrial dysfunction-driven chondrocyte senescence is increasingly recognized as a key driver of cartilage degeneration and pathological cartilage-synovium crosstalk. Here, we engineered a biomimetic, programmable nanoplatform, termed CM@THC, by loading hesperidin, a natural flavonoid with potent antioxidant activity, into tetrahedral framework nucleic acids (tFNAs) and subsequently cloaking the nanocomplex with chondrocyte membranes (CMs). This hierarchical design combines the programmable drug-delivery capacity of tFNAs with the homologous targeting and biointerfacial properties of membrane camouflage, thereby improving nanocomplex stability, cellular internalization, and intra-articular retention. Functionally, CM@THC restored redox homeostasis and PINK1/Parkin-associated mitophagy in IL-1β-stimulated chondrocytes, attenuating cellular senescence and extracellular matrix imbalance while limiting the secondary profibrotic activation of fibroblast-like synoviocytes (FLSs). Collectively, these findings establish a membrane-camouflaged tFNA strategy for natural-product delivery and identify CM@THC as a biomimetic, mitochondria-protective nanotherapeutic that disrupts the pathological cartilage-synovium axis in OA.
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