Evidence map›Paper›PMID 39863621›Full record

ArticleScientific reports2025

Fluid flow impacts endothelial-monocyte interactions in a model of vascular inflammatory fibrosis.

Isabelle Linares, Kaihua Chen, Ava Saffren, Mehran Mansouri, Vinay V Abhyankar, Benjamin L Miller, Stefano Begolo, Hani A Awad, James L McGrath

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. The Role of Phagocytic Cells in the Achilles Tendon.International journal of molecular sciences · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Tendon mechanobiology in the context of tendon biofabrication.Frontiers in bioengineering and biotechnology · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Isabelle LinaresDepartment of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
Kaihua ChenDepartment of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
Ava SaffrenDepartment of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
Mehran MansouriDepartment of Biomedical Engineering, Rochester Institute of Technology, Rochester, NY, USA.
Vinay V AbhyankarDepartment of Biomedical Engineering, Rochester Institute of Technology, Rochester, NY, USA.
Benjamin L MillerDepartment of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
Stefano BegoloALine Inc, Signal Hill, CA, USA.
Hani A AwadDepartment of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
James L McGrathDepartment of Biomedical Engineering, University of Rochester, Rochester, NY, USA. jmcgrath@ur.rochester.edu.

Funding

A microphysiological system of tendon inflammation and fibrosis for drug screening and efficacy testingUH3TR003281 · NCATS · UNIVERSITY OF ROCHESTER · PI AWAD, HANI A, MCGRATH, JAMES L · 2022 to 2024
$2.2M
NCATS NIH HHS UH3 TR003281U.S. Department of Health & Human Services | NIH | National Center for Advancing Translational Sciences (NCATS) UH3TR003281
6 · The paper itself

Abstract

The aberrant vascular response associated with tendon injury results in circulating immune cell infiltration and a chronic inflammatory feedback loop leading to poor healing outcomes. Studying this dysregulated tendon repair response in human pathophysiology has been historically challenging due to the reliance on animal models. To address this, our group developed the human tendon-on-a-chip (hToC) to model cellular interactions in the injured tendon microenvironment; however, this model lacked the key element of physiological flow in the vascular compartment. Here, we leveraged the modularity of our platform to create a fluidic hToC that enables the study of circulating immune cell and vascular crosstalk in a tendon injury model. Under physiological shear stress consistent with postcapillary venules, we found a significant increase in the endothelial leukocyte activation marker intercellular adhesion molecule 1 (ICAM-1), as well as enhanced adhesion and transmigration of circulating monocytes across the endothelial barrier. The addition of tissue macrophages to the tendon compartment further increased the degree of circulating monocyte infiltration into the tissue matrix. Our findings demonstrate the importance of adding physiological flow to the human tendon-on-a-chip, and more generally, the significance of flow for modeling immune cell interactions in tissue inflammation and disease.

Indexed as

Cell CommunicationEndothelial CellsEndothelium, VascularInflammationMonocytesCell AdhesionFibrosisHumansIntercellular Adhesion Molecule-1Lab-On-A-Chip DevicesMacrophagesIntercellular Adhesion Molecule-1FibrosisFluidic shear stressInflammationMicrophysiological systemsMonocyte transmigrationVascular barriers

Identifiers

PMID39863621
PMCPMC11763004

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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 OpenQuestion graph.