Evidence mapPaperPMID 42113993Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2026

Synovial fibroblasts modulate endothelial activation in an acute injury-on-a-chip model.

Hannah M Zlotnick, Declan N Goddard, Christopher J Calo, Abhishek P Dhand, Matthew D Davidson, Aina Solsona-Pujol, Jonathan T Makhoul, Hannah K Weppner, Melissa Wong, Carla R Scanzello and 2 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Hannah M ZlotnickBioFrontiers Institute, University of Colorado Boulder, Boulder, CO 80303.ORCID 0000-0002-0942-3072
Declan N GoddardBioFrontiers Institute, University of Colorado Boulder, Boulder, CO 80303.
Christopher J CaloDepartment of Chemical and Biological Engineering, University of Colorado Boulder, Boulder, CO 80303.
Abhishek P DhandDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104.
Matthew D DavidsonBioFrontiers Institute, University of Colorado Boulder, Boulder, CO 80303.
Aina Solsona-PujolBioFrontiers Institute, University of Colorado Boulder, Boulder, CO 80303.
Jonathan T MakhoulBioFrontiers Institute, University of Colorado Boulder, Boulder, CO 80303.ORCID 0009-0006-0996-7914
Hannah K WeppnerDepartment of Chemical and Biological Engineering, University of Colorado Boulder, Boulder, CO 80303.ORCID 0009-0007-9020-2210
Melissa WongBioFrontiers Institute, University of Colorado Boulder, Boulder, CO 80303.
Carla R ScanzelloCartilage Regeneration using Advanced Technologies to Enable Motion Center, Corporal Michael J. Crescenz VA Medical Center, Philadelphia, PA 19104.ORCID 0000-0002-9290-188X
Laurel E HindDepartment of Chemical and Biological Engineering, University of Colorado Boulder, Boulder, CO 80303.ORCID 0000-0002-2791-668X
Jason A BurdickBioFrontiers Institute, University of Colorado Boulder, Boulder, CO 80303.ORCID 0000-0002-2006-332X

Funding

Dynamic Fibrous Scaffolds for Repairing Dense Connective TissuesR01AR056624 · NIAMS · UNIVERSITY OF PENNSYLVANIA · 2022 to 2025
$2.1M
Interdisciplinary Training in Musculoskeletal ResearchT32AR080630 · UNIVERSITY OF COLORADO DENVER · 2025 to 2025
$360k
CU Boulder CHER4U Program N/ACU Boulder Uplift Program N/AHHS | National Institutes of Health (NIH) R01AR056624HHS | National Institutes of Health (NIH) T32AR080630National Science Foundation (NSF) CMMI: 15-48571NCRR NIH HHS S10 RR026680NIAMS NIH HHS R01 AR056624NIAMS NIH HHS T32 AR080630Schmidt Family Foundation (SFF) N/A
6 · The paper itself

Abstract

Most patients who sustain an acute joint injury develop degenerative joint disease or osteoarthritis (OA). Animal models have informed the design of OA therapeutics; however, no disease-modifying therapy has successfully translated to human patients. Thus, there is a strong motivation to develop humanized in vitro platforms to fill a critical gap in knowledge of disease progression postinjury. Here, we develop an acute injury-on-a-chip model of the synovium, a vascularized, joint-lining tissue that has been implicated in OA progression and as a key driver of joint disease. We apply this chip-based system to investigate the crosstalk between endothelial cells, lining an engineered vessel, and synovial fibroblasts, embedded within an extracellular matrix hydrogel. Our data indicate that synovial fibroblasts, rather than initiating disease, attempt to support and maintain vascular function in the presence of acute inflammation (i.e., interleukin-1β). Such knowledge may provide new targets for OA therapeutics, preventing the progression from joint injury to disease in patients.

Indexed as

Endothelial CellsFibroblastsLab-On-A-Chip DevicesSynovial MembraneAnimalsExtracellular MatrixHumansInterleukin-1betaMicrophysiological SystemsOsteoarthritisInterleukin-1betaacute injurycrosstalksynoviumtissue-on-a-chipvasculature

Identifiers

PMID42113993
PMCPMC13170127

What Socratic holds

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Registered trials

None linked

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.