ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Targeted Inhibition of CD74
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 8 papers.
What it found
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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
8 citing papers in PubMed.
- Immunomodulatory thermosensitive hydroxypropyl chitin hydrogel platform maintains cartilage-synovium homeostasis for enhanced osteoarthritis therapy.Bioactive materials · 2026Article
- S2P-modified PLGA bifunctional nanodrug: inhibiting vascular senescence and foam cell formation for atherosclerosis treatment.Journal of nanobiotechnology · 2026Article
- Multi-omics mapping identifies a C/EBPβ-S100a4⁺ macrophage axis as a therapeutic target in acute spinal cord injury.Journal of translational medicine · 2026Article
- Wine-Processed Cornus officinalis Ameliorates Osteoarthritis via Modulating M1/M2 Macrophage Polarization.Journal of cellular and molecular medicine · 2026Article
- Poricoic Acid A Attenuates Osteoarthritis Progression by Stabilizing PTEN and Suppressing PI3K/AKT Signaling.International journal of molecular sciences · 2026Article
- Targeted Inhibition of CD74Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Research progress on the role of CD14 in osteoarthritis.Frontiers in immunology · 2026Review
- Luteolin and neuroinflammation: a multi-target therapeutic strategy for central nervous system disorders.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Synovial inflammation represents a hallmark pathological process in osteoarthritis (OA), yet the cellular drivers orchestrating this response remain incompletely defined. Through single-cell transcriptomic profiling of human OA synovial tissues, a distinct subset of CD74⁺ macrophages is identified that displayed robust pro-inflammatory transcriptional signatures, underscoring the pivotal role of macrophages in shaping the inflammatory microenvironment. To explore therapeutic opportunities, computational ligand-target interaction analysis predicted luteolin as a high-affinity binder of CD74. Mechanistically, luteolin suppressed CD74 expression and disrupted the assembly of the CEBPB-p65 complex, thereby preventing p65 nuclear translocation and subsequent activation of the NF-κB signaling cascade in macrophages. To achieve targeted delivery, a nanoplatform MIF
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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.