Type II collagen as a material-mediated instructive platform: Cartilage regeneration and fibrosis suppression via the Tp63-Cytl1 axis.

Weicong Zhu, Shaojie Liu, Yusheng Liu, Qiguang Zhong, Hanshuo Zhang, Xiaohang Zheng, Jiake Xu, Xiaohong Yang

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Article in Materials today. Bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

8 authors.

Weicong ZhuGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, 510220, PR China.

Shaojie LiuDepartment of Gastrointestinal Surgery, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, 510220, PR China.

Yusheng LiuDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510260, PR China.

Qiguang ZhongDepartment of Gastrointestinal Surgery, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, 510220, PR China.

Hanshuo ZhangDepartment of Gastrointestinal Surgery, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, 510220, PR China.

Xiaohang ZhengShenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, PR China.

Jiake XuShenzhen University of Advanced Technology, Shenzhen, 518055, PR China.

Xiaohong YangGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, 510220, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A major challenge in cartilage regeneration is maintaining the hyaline cartilage phenotype and matrix over time while limiting hypertrophy and fibrosis. Here, type II collagen (Col2)-hyaluronic acid (Col2H) and type I collagen-hyaluronic acid (Col1H) sponges were compared using long-term three-dimensional chondrocyte culture, cross-species transcriptomic analysis, and functional experiments. Col2H supported longer-term chondrocyte phenotype and matrix retention than Col1H. Cytl1 was prioritized because it ranked highly in Col2H-associated analysis and was consistently downregulated during chondrocyte dedifferentiation in human and rat datasets. Functional assays, ChIP-qPCR, and co-immunoprecipitation supported involvement of an Itgb8-Nov-Tp63-Cytl1 regulatory network in the Col2-associated response. Col2H also showed preliminary cartilage-repair potential in a rabbit defect model. In human osteoarthritis cartilage, a five-gene signature comprising Cytl1, Tp63, Nov, Itgb8, and TIMP3 showed internal stability and an association with histological severity. These findings support a material-associated regulatory role for Col2H in chondrocyte phenotype and matrix maintenance.

Indexed as

Bioactive scaffoldsCartilage matrix maintenanceChondrocyte phenotype maintenanceECM signalingType II collagen

Identifiers

PMID42861271

DOI10.1016/j.mtbio.2026.103700

PMCPMC13654500

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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.