ArticleArthritis & rheumatology (Hoboken, N.J.)2026
Monocyte-Derived Macrophages-Synovial Fibroblasts Crosstalk Unravels Oncostatin Signaling Network as a Driver of Synovitis in Osteoarthritis.
Article in Arthritis & rheumatology (Hoboken, N.J.), 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 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
8 citing papers in PubMed.
- Multi‑omics integration in osteoarthritis: Unraveling cell‑type‑specific gene‑metabolite networks for precision medicine (Review).International journal of molecular medicine · 2026Review
- PAD4 deletion in synovial macrophages exacerbates pathology in inflammatory arthritis.Research square · 2026Article
- A biomimetic nanoplatform enables shTHY1-mediated immunomodulation and cartilage remodeling for osteoarthritis therapy.Materials today. Bio · 2026Article
- Molecular mediators of motion: RNA-RBP networks in exercise-induced osteoarthritis protection.Frontiers in genetics · 2026Review
- Epigenetic regulation in osteoarthritis: recent updates and emerging mechanisms.Frontiers in genetics · 2026Review
- Research progress on the role of CD14 in osteoarthritis.Frontiers in immunology · 2026Review
- Synovial immune control failure in osteoarthritis: from maintenance of tissue homeostasis to inflammatory niche formation.Frontiers in immunology · 2026Review
- Mechanisms of synovial macrophage polarization in osteoarthritis pathogenesis and their therapeutic implications.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
objectiveOsteoarthritis (OA) is a debilitating joint disease that is characterized by cartilage degradation, synovial inflammation, and pain. Macrophages have been implicated in OA pathology, but the origins and functions of diverse macrophage subsets seeding the synovial joint tissue remain incompletely understood. This study investigates macrophage heterogeneity, ontogeny, fate, and communication with stromal niche cells in OA.
methodsSingle-cell RNA sequencing was employed on synovial cells isolated from mice with collagenase-induced OA (CiOA) and CD14
resultsThree macrophage subsets with distinct gene signatures and origins were identified in CiOA, including contributions to synovial inflammation and tissue remodeling. Fate mapping via CCR2-creER and CX3CR1-creER mice revealed the expansion of monocyte-derived TIM4
conclusionOur study provides insights into macrophage subsets and their interplay with the joint microenvironment, bridging the gap between their origins, transcriptomic profiles, and roles in OA. Specifically, the OSM/OSMR axis represents a pivotal mechanism in recruited macrophage-fibroblast crosstalk, offering potential targets for novel biomarkers and therapies to manage OA-related synovitis.
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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.