ArticleScience advances2026
Aptamer-functionalized apoptotic vesicles ameliorate osteoarthritis via resuming mitochondria OXPHOS of chondrocytes.
Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Immunometabolic reprogramming in osteoporosis-osteoarthritis comorbidity: from inflammaging to osteochondral unit degeneration.Frontiers in immunology · 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence suggests that osteoarthritis (OA) progression is critically associated with disruptions of cartilage matrix homeostasis caused by mitochondrial impairment in chondrocytes. Apoptotic vesicles (apoVs) derived from mesenchymal stem cells (MSCs) have exhibited great therapeutic promising for tissue regeneration and osteoarticular diseases. However, their poor ability targeting chondrocytes and short-time retention in joint cavity hinder further clinical translation. As a chemically synthesized nucleic acid, aptamer tgg2 demonstrated a robust specificity binding with chondrocytes. In this study, our team successfully functionalized apoVs with tgg2 (tgg2@apoVs) via Schiff base reaction with high conjugation efficiency and fabricated an injectable sustained-release system based on hyaluronic acid methacryloyl (HAMA) hydrogels. tgg2@apoVs significantly promoted chondrocyte extracellular matrix synthesis and improved mitochondrial oxidative phosphorylation (OXPHOS) in vitro. The HAMA injectable hydrogels compounded with tgg2@apoVs remarkedly alleviated OA symptoms in vivo. The potential molecular mechanism of apoVs' improvement in mitochondrial energy metabolism of chondrocytes is preliminarily investigated. Specifically, apoVs activate transcriptional factor Yin Yang 1 (YY1) to up-regulate the expression of Cox7c, a key subunit of complex IV in electron transport chain, thereby augmenting mitochondrial OXPHOS. In conclusion, the tgg2@apoVs' sustained-release system provides a cost-effective solution for OA treatment, and the elucidation of the molecular mechanism underlying apoVs' enhancement of chondrocyte OXPHOS offers insights for broader applications in energy metabolism-related diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.