ArticleAmerican journal of human genetics2024
Primary cartilage transcriptional signatures reflect cell-type-specific molecular pathways underpinning osteoarthritis.
Article in American journal of human genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A Principle-Guided Multistep Workflow for Screening Potential Quality Marker Candidates of Sanqi Shangyao Tablet Based on UHPLC-Q-Orbitrap MS, In Silico Screening, and In Vitro Validation.Biomedical chromatography : BMC · 2026Article
- Transcriptome analysis in osteoarthritis primary tissues identifies high-confidence effector genes.Nature communications · 2026Article
- Dissecting the genetic architecture of knee alignment reveals its contribution to osteoarthritis risk.medRxiv : the preprint server for health sciences · 2026Article
- Single-cell RNA sequencing of healthy and diseased rat temporomandibular joint condyle cartilage.PloS one · 2026Article
- Forkhead box O proteins in chondrocyte aging and diseases.Journal of orthopaedic translation · 2025Review
- Identification of Genes Linked to Meniscal Degeneration in Osteoarthritis: An In Silico Analysis.International journal of molecular sciences · 2025Article
- Article
- Ferroptosis-related genes and pathways in knee osteoarthritis cartilage degeneration: discovered by bioinformatics technology and in vivo experimental verification.American journal of translational research · 2025Article
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Authors and funding
11 authors.
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Abstract
Translational efforts in osteoarthritis are hampered by a gap in our understanding of disease processes at the molecular level. Here, we present evidence of pronounced transcriptional changes in high- and low-disease-grade cartilage tissue, pointing to embryonic processes involved in disease progression. We identify shared transcriptional programs between osteoarthritis cartilage and cell populations in the human embryonic and fetal limb, pointing to increases in pre-hypertrophic chondrocytes' transcriptional programs in low-grade cartilage and increases in osteoblastic signatures in high-grade disease tissue. We find that osteoarthritis genetic risk signals are enriched in six gene co-expression modules and show that these transcriptional signatures reflect cell-type-specific expression along the endochondral ossification developmental trajectory. Using this network approach in combination with causal inference analysis, we present evidence of a causal effect on osteoarthritis risk for variants associated with the expression of ten genes that have not been previously reported as effector genes in genome-wide association studies in osteoarthritis. Our findings point to key molecular pathways as drivers of cartilage degeneration and identify high-value drug targets and repurposing opportunities.
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