ArticleOsteoarthritis and cartilage open2025
Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation.
Article in Osteoarthritis and cartilage open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Protocol for the enrichment of endosteal and periosteal mesenchymal cells from murine bone for single-cell transcriptome analysis.STAR protocols · 2026Article
- Exploring the Senotherapeutic Potential of Polyphenols in Aging and Disease: A Literature Review.International journal of molecular sciences · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
Objective: Cellular senescence has been implicated in the progression of post-traumatic osteoarthritis, but any role in pre-osteoarthritic cartilage repair is unknown. Our objective was to determine whether senescent cells contribute to fibrocartilage repair using a rodent model of marrow stimulation. Design: A 1 mm osteochondral defect was generated in the trochlear groove of young adult and middle-aged Lewis rats, modeling the age range when humans receive marrow stimulation. Some rats were treated by intra-articular (IA) injection of senolytic drugs navitoclax or dasatinib plus quercetin. Repair tissue was characterized during the first months after marrow stimulation by histology as well as bulk and single cell transcriptomic analysis. Results: Multiple senescence markers were measured within repair tissue during the first months of repair, in contrast to adjacent, intact articular cartilage. The IA delivery of senolytic drugs reduced p16 Conclusions: Senescent cells, including neochondrocytes, are abundant within inferior repair tissue following marrow stimulation. While their fibrogenic SASP is associated with poor healing, their removal after senescence induction does not improve repair tissue quality, possibly due to the lack of a replacement chondrogenic population.
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Registered trials
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