ArticleJournal of nanobiotechnology2025
Effectively alleviate rheumatoid arthritis via maintaining redox balance, inducing macrophage repolarization and restoring homeostasis of fibroblast-like synoviocytes by metformin-derived carbon dots.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Dysregulation of the DNA repair‑immune axis: Targeted therapeutic strategies for autoimmune diseases (Review).International journal of molecular medicine · 2026Review
- Application of hyperbaric oxygen therapy in the treatment of spinal cord injury: insights from preclinical to clinical evidence.Medical gas research · 2026Review
- Smart Polymer Nanoparticles: Targeting Macrophages/Fibroblasts and Modulating the Microenvironment for Rheumatoid Arthritis Therapy.International journal of nanomedicine · 2026Review
- Immunological heterogeneity in rheumatoid arthritis: challenges in early-stage stratification, non-response to targeted therapy, and the restoration of immune tolerance.Frontiers in immunology · 2026Review
- Nanomaterial-Based Photothermal Therapy for Inflammatory Diseases: Intervention Strategies, Synergistic Effects, and Future Challenges.International journal of nanomedicine · 2026Review
- Ferroptosis as a therapeutic nexus: traditional Chinese medicine interventions in rheumatoid arthritis.Frontiers in immunology · 2026Review
- Immunometabolism in rheumatoid arthritis: mechanisms, biomarkers, and the path to precision medicine.Frontiers in immunology · 2026Review
- Antidiabetic Agents as Antioxidant and Anti-Inflammatory Therapies in Neurological and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Fisetin carbon dots alleviate periodontitis by enhancing mitophagy through regulation of sirtuin 3 SUMOylation.Journal of nanobiotechnology · 2025Article
- Polyhexamethylene guanidine derived carbon dots with antibacterial and immunoregulatory properties loaded on carboxymethyl chitosan and ε-poly-L-lysine hydrogel to achieve sustained drug release for treatingMaterials today. Bio · 2025Article
- Synovium-On-A-Chip: Simulating the Microenvironment of the Rheumatoid Arthritis Synovium via Multicell Interactions to Target Fibroblast-Like Synoviocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- NLRP3 Inflammasome-Mediated Pyroptosis in Osteoporosis: Osteoimmune Mechanisms and Therapeutic Targeting.Journal of cellular and molecular medicine · 2025Review
- Carbon dots-based drug delivery for bone regeneration.Frontiers in bioengineering and biotechnology · 2025Review
- Stimuli-Responsive Nanoplatforms for Precision Intervention in Rheumatoid Arthritis.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnologyReview
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overproduction of reactive oxygen species (ROS), elevated synovial inflammation, synovial hyperplasia and fibrosis are the main characteristic of microenvironment in rheumatoid arthritis (RA). Macrophages and fibroblast-like synoviocytes (FLSs) play crucial roles in the progression of RA. Hence, synergistic combination of ROS scavenging, macrophage polarization from pro-inflammatory M1 phenotype towards M2 anti-inflammatory phenotype, and restoring homeostasis of FLSs will provide a promising therapeutic strategy for RA. In this study, we successfully synthesized metformin-derived carbon dots (MCDs), and investigated the antirheumatic effect in vivo and in vitro. Designed MCDs could target inflamed cells and accumulate at the inflammatory joints of collagen-induced arthritis (CIA) rats. In vivo therapeutic investigation suggested that MCDs reduced synovial inflammation and hyperplasia, ultimately prevented cartilage destruction, bone erosion, and synovial fibrosis in CIA rats. In addition, MCDs eliminated the cellular ROS in M1 phenotype macrophages in RA microenvironment through the enzyme-like catalytic activity as well as inhibiting NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome signaling pathway, effectively polarizing them into the M2 phenotype to realize the anti-inflammatory effect. Furthermore, MCDs could inhibit the proliferation, migration, and fibrosis of inflamed FLSs. Mechanistically, MCDs restored the homeostasis of FLSs while reducing the level of synovial inflammation by blocking IL-6/gp130 signaling pathway. Combined with preferable biocompatibility, MCDs offer a prospective treatment approach for RA.
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