Evidence map›Paper›PMID 39716911›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Microphysiological System-Generated Physiological Shear Forces Reduce TNF-α-Mediated Cartilage Damage in a 3D Model of Arthritis.

Alexandra Damerau, Duc Ha Do Nguyen, Christina Lubahn, Kasper Renggli, Moritz Pfeiffenberger, Gerhard Krönke, Matthias Herrmann, Thomas Leeuw, Frank Buttgereit, Timo Gaber

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Observational
  6. Article
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

10 authors.

Alexandra DamerauDepartment of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany.ORCID https://orcid.org/0000-0001-6651-2963
Duc Ha Do NguyenDepartment of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany.
Christina LubahnDepartment of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany.
Kasper RenggliSchool of Life Sciences, University of Applied Sciences and Arts Northwestern Switzerland, Muttenz, 4132, Switzerland.ORCID https://orcid.org/0000-0001-6865-4084
Moritz PfeiffenbergerDepartment of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany.ORCID https://orcid.org/0000-0001-6327-2343
Gerhard KrönkeDepartment of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany.ORCID https://orcid.org/0000-0002-7566-4325
Matthias HerrmannImmunology & Inflammation Research TA, Sanofi-Aventis Deutschland GmbH, 65926, Frankfurt, Germany.
Thomas LeeuwImmunology & Inflammation Research TA, Sanofi-Aventis Deutschland GmbH, 65926, Frankfurt, Germany.
Frank ButtgereitDepartment of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany.ORCID https://orcid.org/0000-0003-2534-550X
Timo GaberDepartment of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany.ORCID https://orcid.org/0000-0002-6675-3895

Funding

Joachim Herz StiftungSanofi Aventis Deutschland GmbHStudienstiftung des Deutschen Volkes
6 · The paper itself

Abstract

Osteoarthritis (OA) is a leading cause of disability, often resulting from overuse or injury, but inactivity can also contribute to cartilage degeneration. Conventional in vivo models struggle to isolate and study the specific effects of mechanical stress on cartilage health. To address this limitation, a microphysiological system (MPS) is established to examine how varying levels of shear stress impact cartilage homeostasis. The system allows for the cultivation of 3D chondrogenic microconstructs (CMCs) derived from human mesenchymal stromal cells, simulating both physiological and pathophysiological shear stress. Inflammation is induced via TNF-α or activated peripheral blood mononuclear cells to model cartilage damage, enabling the evaluation of therapeutic interventions. The study demonstrates the development of an arthritis-like phenotype and successful restoration of cartilage conditions through a JAK inhibitor under physiological shear stress. Physiological shear stress is identified as a critical factor in maintaining cartilage integrity. This MPS offers a standardized method to study shear stress, replicate cytokine-induced cartilage damage, and simulate key features of arthritis, providing a valuable alternative to animal models.

Indexed as

Cartilage, ArticularOsteoarthritisTumor Necrosis Factor-alphaHumansMesenchymal Stem CellsMicrophysiological SystemsStress, MechanicalTumor Necrosis Factor-alphaarticular cartilage breakdownchondrogenic 3D modelimmune cellsmatrix degenerationmesenchymal stromal cellmicrofluidic systempro‐inflammatory cytokineTNF‐α

Identifiers

PMID39716911
PMCPMC11831510

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.