ArticleJournal of cellular and molecular medicine2024
PLCγ1 deficiency in chondrocytes accelerates the age-related changes in articular cartilage and subchondral bone.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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.
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Who cites it
4 citing papers in PubMed.
- Potential link between Gordonibacter pamelaeae and phospholipase C gamma 1 in osteoarthritis.AMB Express · 2026Article
- Integrated analysis of single-cell RNA sequencing, transcriptomics, and thermal proteome profiling identifies PLCG1 as the therapeutic target of isopimpinellin in treating rheumatoid arthritis.Cellular & molecular biology letters · 2026Article
- PLCγ1 deficiency in chondrocytes accelerates the age-related changes in articular cartilage and subchondral bone.Journal of cellular and molecular medicine · 2024Article
- Nasoseptal chondroprogenitors isolated through fibronectin-adherence confer no biological advantage for cartilage tissue engineering compared to nasoseptal chondrocytes.Frontiers in bioengineering and biotechnology · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Ageing is the most prominent risk for osteoarthritis (OA) development. This study aimed to investigate the role of phosphoinositide-specific phospholipase Cγ (PLCγ) 1, previously linked to OA progression, in regulating age-related changes in articular cartilage and subchondral bone. d-galactose (d-Gal) was employed to treat chondrocytes from rats and mice or injected intraperitoneally into C57BL/6 mice. RTCA, qPCR, Western blot and immunohistochemistry assays were used to evaluate cell proliferation, matrix synthesis, senescence genes and senescence-associated secretory phenotype, along with PLCγ1 expression. Subchondral bone morphology was assessed through micro-CT. In mice with chondrocyte-specific Plcg1 deficiency (Plcg1
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Registered trials
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