ArticleBone reports2023
Bone-cartilage crosstalk informed by aging mouse bone transcriptomics and human osteoarthritis genome-wide association studies.
Article in Bone reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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
6 citing papers in PubMed, 8 citations in OpenAlex.
- Structural and functional changes in articulating joints during aging of male and female C57BL/6JN mice.Osteoarthritis and cartilage · 2026Article
- USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy.JBMR plus · 2026Article
- Complement factor D (adipsin) mediates pressure-pain hypersensitivity post destabilization of medial meniscus injury.Arthritis research & therapy · 2025Article
- Effect of Passaging on Bovine Chondrocyte Gene Expression and Engineered Cartilage Production.Tissue engineering. Part A · 2024Article
- Three decades of advancements in osteoarthritis research: insights from transcriptomic, proteomic, and metabolomic studies.Osteoarthritis and cartilage · 2024Review
- Genetic and Gene Expression Resources for Osteoporosis and Bone Biology Research.Current osteoporosis reports · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Subchondral bone participates in crosstalk with articular cartilage to maintain joint homeostasis, and disruption of either tissue results in overall joint degeneration. Among the subchondral bone changes observed in osteoarthritis (OA), subchondral bone plate (SBP) thickening has a time-dependent relationship with cartilage degeneration and has recently been shown to be regulated by osteocytes. Here, we evaluate the effect of age on SBP thickness and cartilage degeneration in aging mice. We find that SBP thickness significantly increases by 18-months of age, corresponding temporally with increased cartilage degeneration. To identify factors in subchondral bone that may participate in bone cartilage crosstalk or OA, we leveraged mouse transcriptomic data from one joint tissue compartment - osteocyte-enriched bone - to search for enrichment with human OA in UK Biobank and Arthritis Research UK Osteoarthritis Genetics (arcOGEN) GWAS using the mouse2human (M2H, www.mouse2human.org) strategy. Genes differentially expressed in aging mouse bone are significantly enriched for human OA, showing joint site-specific (knee vs. hip) relationships, exhibit temporal associations with age, and unique gene clusters are implicated in each type of OA. Application of M2H identifies genes with known and unknown functions in osteocytes and OA development that are clinically associated with human OA. Altogether, this work prioritizes genes with a potential role in bone/cartilage crosstalk for further mechanistic study based on their association with human OA in GWAS.
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Registered trials
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.