ArticleProceedings of the National Academy of Sciences of the United States of America2016
Suppression of NF-κB activity via nanoparticle-based siRNA delivery alters early cartilage responses to injury.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 97 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
97 citing papers in PubMed.
- NO-Responsive Oleanolic Acid Self-Assembled Micelles Co-Loaded with BAY 11-7082 for Synergistic Chondroprotection and Anti-Osteoarthritis Therapy.Bioengineering (Basel, Switzerland) · 2026Article
- Localized NF-κB Inhibition Reduces Lipid Nanoparticle-Associated Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Protein Response to ACL Injury in Humans Show Early Cartilage Remodeling and Differences by Sex.bioRxiv : the preprint server for biology · 2026Article
- Review
- Beyond inflammation: siRNA strategies for precision targeting in rheumatological disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Small heterodimer partner protects against osteoarthritis by inhibiting IKKβ/NF-κB-mediated matrix-degrading enzymes in chondrocytes.Nature communications · 2026Article
- Nucleic acid-based therapeutics to restore joint homeostasis in age-related and post-traumatic arthritis.npj biomedical innovations · 2026Review
- MicroRNA-127-3p Inhibits In Vitro Osteogenesis and Dampens Trauma-Induced Heterotopic Ossification In Vivo.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- The influence of PPARγ mediated MAPK and NF-κB activation in AGEs stimulated apoptosis and autophagy in human chondrocytes.Journal of orthopaedics · 2025Article
- Advances in locally administered nucleic acid therapeutics.Bioactive materials · 2025Review
- FSH enhances the inflammatory response of macrophages in the knee joint possibly through the NFκB pathway.FEBS open bio · 2025Article
- Rejuvenating Hyaline Cartilage with Senescence-Targeting Si-ADAM19 Delivery for Osteoarthritis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Macrophage SUCLA2 coupled glutaminolysis manipulates obesity through AMPK.Nature communications · 2025Article
- 1,25(OH)Clinical rheumatology · 2025Article
- Therapeutic Controlled Release Strategies for Human Osteoarthritis.Advanced healthcare materials · 2025Review
- siRNAs, tRNAs, and rRNAs in Osteoarthritis: Biological Functions and Therapeutic Opportunities.Biologics : targets & therapy · 2025Review
- Nanomaterial-Based Drug Delivery Systems Targeting Functional Cells for Osteoarthritis Treatment: Mechanisms, Challenges and Future Prospects.International journal of nanomedicine · 2025Review
- Augmented expression of superoxide dismutase 2 mitigates progression and rupture of experimental abdominal aortic aneurysm.Theranostics · 2025Article
- Engineering gene-activated bioprinted scaffolds for enhancing articular cartilage repair.Materials today. Bio · 2024Review
- Mode of injury and level of synovitis alter inflammatory chondrocyte gene expression and associated pathways.Scientific reports · 2024Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
Osteoarthritis (OA) is a major cause of disability and morbidity in the aging population. Joint injury leads to cartilage damage, a known determinant for subsequent development of posttraumatic OA, which accounts for 12% of all OA. Understanding the early molecular and cellular responses postinjury may provide targets for therapeutic interventions that limit articular degeneration. Using a murine model of controlled knee joint impact injury that allows the examination of cartilage responses to injury at specific time points, we show that intraarticular delivery of a peptidic nanoparticle complexed to NF-κB siRNA significantly reduces early chondrocyte apoptosis and reactive synovitis. Our data suggest that NF-κB siRNA nanotherapy maintains cartilage homeostasis by enhancing AMPK signaling while suppressing mTORC1 and Wnt/β-catenin activity. These findings delineate an extensive crosstalk between NF-κB and signaling pathways that govern cartilage responses postinjury and suggest that delivery of NF-κB siRNA nanotherapy to attenuate early inflammation may limit the chronic consequences of joint injury. Therapeutic benefits of siRNA nanotherapy may also apply to primary OA in which NF-κB activation mediates chondrocyte catabolic responses. Additionally, a critical barrier to the successful development of OA treatment includes ineffective delivery of therapeutic agents to the resident chondrocytes in the avascular cartilage. Here, we show that the peptide-siRNA nanocomplexes are nonimmunogenic, are freely and deeply penetrant to human OA cartilage, and persist in chondrocyte lacunae for at least 2 wk. The peptide-siRNA platform thus provides a clinically relevant and promising approach to overcoming the obstacles of drug delivery to the highly inaccessible chondrocytes.
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