Evidence map›Paper›PMID 42263900›Full record

ArticleActa biomaterialia2026

Decorin promotes nascent proteoglycan retention in cartilage matrix by strengthening collagen II-aggrecan integration.

Thomas Li, Gabriela Canziani, Yuchen Liu, Neil Patel, Biao Han, Mingyue Fan, Annie Porter, Bryan Kwok, Chao Wang, Qing Li and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Acta biomaterialia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Nascent Extracellular Matrix Converts Biomaterial Cues into Cell Fate Decisions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Thomas LiSchool of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, United States.
Gabriela CanzianiDepartment of Biochemistry and Molecular Biology, College of Medicine, Drexel University, Philadelphia, PA 19102, United States.
Yuchen LiuSchool of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, United States.
Neil PatelSchool of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, United States.
Biao HanSchool of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, United States.
Mingyue FanSchool of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, United States.
Annie PorterDepartment of Mechanical Engineering, University of Delaware, Newark, DE 19716, United States.
Bryan KwokSchool of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, United States.
Chao WangSchool of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, United States.
Qing LiSchool of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, United States.
David E BirkDepartment of Molecular Pharmacology and Physiology, Morsani School of Medicine, University of South Florida, Tampa, FL 33612, United States.
Renato V IozzoDepartment of Pathology and Genomic Medicine, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA 19107, United States.
Irwin M ChaikenDepartment of Biochemistry and Molecular Biology, College of Medicine, Drexel University, Philadelphia, PA 19102, United States.
X Lucas LuDepartment of Mechanical Engineering, University of Delaware, Newark, DE 19716, United States.
Robert L MauckMcKay Orthopaedic Research Laboratory, Department of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States; CReATE Motion Center, Corporal Michael J. Crescenz Veterans Administration Medical Center, Philadelphia, PA 19104, United States.
Lin HanSchool of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, United States. Electronic address: lh535@drexel.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cartilage extracellular matrix (ECM), a hydrated collagen II-aggrecan composite, undergoes dynamic turnover during both normal homeostasis and disease-associated remodeling. This study elucidates a crucial role for decorin in promoting the retention and stability of nascent aggrecan within this matrix. By applying bio-orthogonal click-labeling, we demonstrate that loss of decorin accelerates the release of nascent aggrecan under both physiological and inflammatory conditions, without affecting its preferential localization to the pericellular matrix. Conversely, supplementation with exogenous decorin mitigates inflammation-induced loss of nascent aggrecan, supporting its potential as a therapeutic target. At the molecular level, decorin exhibits strong binding affinity for aggrecan, and enhances aggrecan-aggrecan and aggrecan-collagen II interactions, reinforcing its direct role in integrating cartilage matrix constituents. Also, by binding to collagen II, decorin stiffens the collagen II fibril network, thereby strengthening the confinement effect that limits the diffusive loss of entrapped aggrecan. Notably, decorin does not alter chondrocyte transcriptomic profiles in vivo, emphasizing its primary role in maintaining matrix integrity through biophysical mechanisms rather than cell signaling. Together, these findings provide a mechanistic foundation for developing decorin-based biomaterials or gene therapies aimed at preserving or regenerating the cartilage matrix for improved outcomes in osteoarthritis. STATEMENT OF SIGNIFICANCE: Development of effective cartilage repair strategies is challenged by the limited understanding of molecular events that regulate the dynamic turnover and degenerative changes of cartilage extracellular matrix. This study shows that decorin, a small proteoglycan, promotes the retention and stability of nascent aggrecan within both normal and degenerative cartilage matrix by augmenting the integration between collagen II and aggrecan molecules and strengthening the collagen II fibril network. In turn, exogenous decorin mitigates the accelerated loss of nascent aggrecan instigated by inflammatory stimulation. Collectively, these findings establish decorin as a therapeutic target for preserving cartilage matrix integrity and improving osteoarthritis intervention.

Indexed as

AggrecansCartilageCartilage, ArticularCollagen Type IIDecorinExtracellular MatrixProteoglycansAnimalsChondrocytesAggrecansCollagen Type IIDecorinProteoglycansBiomacromolecular assemblyClick-labelingDecorinExtracellular matrixProteoglycans

Identifiers

PMID42263900

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.