ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Biocatalytic Nanoregulators Restore Joint Redox-Immune Homeostasis in Rheumatoid Arthritis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Biocatalytic Nanoregulators Restore Joint Redox-Immune Homeostasis in Rheumatoid Arthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Nanomedicine Strategies for Rheumatoid Arthritis: Precision Delivery and Immune Microenvironment Modulation.International journal of nanomedicine · 2026Review
- Extracellular vesicle-mediated immunomodulation and targeted delivery: breakthroughs and challenges in rheumatoid arthritis therapy.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Rheumatoid arthritis (RA), a debilitating autoimmune disorder marked by progressive synovitis and osteochondral erosion, presents critical therapeutic challenges due to the limitations of existing regimens, including non-specific biodistribution and compromised risk-benefit profiles. In this study, a novel therapeutic approach is proposed utilizing mesenchymal stem cell-derived extracellular vesicles (EVs) coating on ruthenium-loaded metal-organic frameworks (Ru@ZrMOF), which exhibit catalase mimetic activities. The EVs coating enhances the biocompatibility and targeting efficiency of the Ru@ZrMOF, while also promoting cartilage protection. Through reactive oxygen species (ROS) scavenging and oxygen production, Ru@ZrMOF/EVs significantly alleviate joint inflammation, promote cartilage protection, and inhibit pannus formation. The therapeutic mechanism involves polarization of macrophages from the M1 pro-inflammatory phenotype to the M2 anti-inflammatory phenotype, facilitating a shift in cytokine profiles from pro-inflammatory to anti-inflammatory, and downregulation of hypoxia inducible factor-1α. These findings demonstrate that Ru@ZrMOF/EVs offer a promising strategy for RA treatment by addressing both inflammation and tissue protection through targeted ROS regulation and immune modulation.
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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.