ArticleMolecular systems biology2025
Synovial matrix turnover controls immune cell spatial patterning in inflammation resolution.
Article in Molecular systems biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- TLR2 inhibition attenuates NET-driven inflammation and restenosis during poly-lactic acid bioresorbable scaffold degradation.Bioactive materials · 2026Article
- Targeting fibroblasts in immune mediated inflammatory diseases: a cellular basis for cure?Rheumatology (Oxford, England) · 2026Review
- Review
- Integrative analysis of single-cell and bulk RNA sequencing data using machine learning identifies PTGDS as a key subsynovial fibroblast gene in osteoarthritis.Journal of molecular histology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
Immune-mediated inflammatory diseases remain plagued by poor treatment responses and lack curative therapies. Convergent findings suggest a role for the stromal compartment and extracellular matrix composition dysregulation. Using rheumatoid arthritis as a model, we define an analytical pipeline combining transcriptomic, proteomic and degradomic analysis to characterise disease activity-specific matrix perturbations. This revealed synergistic contributions from fibroblasts and myeloid cells to matrix composition, with fibroblast subsets defining distinct subsynovial niches through distinct matrix expression profiles. Transcriptional dysregulation of collagen VI was found to be a feature of RA activity, with collagen VI protein accumulation linked to remission-associated states. Spatial analysis and in vitro migration showed collagen VI inhibits immune ingress, confining infiltrating cells to perivascular pockets termed "COL6 dark" zones. Matrix degradation-associated monocytes were found at the leading edge of these zones, expanding immune-permissive niches, and releasing RA-associated collagen VI fragments. Our work reveals how dynamic matrix remodelling can in turn limit, and enable, cell immigration in RA, identifying a new mechanism controlling tissue-level disease activity.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.