ArticleAnnals of translational medicine2022
A transcriptome-wide association study provides new insights into the etiology of osteoarthritis.
Article in Annals of translational medicine, 2022. 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.
- Selective chr21 homolog silencing reveals polymorphisms influence the epigenetic silencing and functional dosage of RWDD2B.American journal of human genetics · 2026Article
- Selective chr21 homolog silencing reveals polymorphisms influence the epigenetic silencing and functional dosage of RWDD2B.bioRxiv : the preprint server for biology · 2025Article
- Systematic druggable genome-wide Mendelian randomization identifies therapeutic targets for calcium pyrophosphate deposition disease.Clinical rheumatology · 2025Article
- Identification of Association Between Mitochondrial Dysfunction and Sarcopenia Using Summary-Data-Based Mendelian Randomization and Colocalization analyses.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- Low-dose Radiation Therapy (LDRT) in Managing Osteoarthritis: A Comprehensive Review.Current therapeutic research, clinical and experimental · 2025Review
- A splicing-based multitissue association study of joint transcriptomes identified susceptibility genes for osteoarthritis.Frontiers in immunology · 2025Article
- Polymorphism rs143384 GDF5 reduces the risk of knee osteoarthritis development in obese individuals and increases the disease risk in non-obese population.Arthroplasty (London, England) · 2024Article
- Identification of candidate genes and chemicals associated with osteoarthritis by transcriptome-wide association study and chemical-gene interaction analysis.Arthritis research & therapy · 2023Article
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Authors and funding
5 authors.
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Abstract
Background: Osteoarthritis (OA) is a common clinical disease caused by a variety of factors, including genetic variants. Although genome-wide association studies (GWAS) have been performed to elucidate the genetic basis of OA, some loci of risk located in noncoding regions of the genome have been neglected. Therefore, we integrated multiple data types to detect the genetic component of gene expression in OA patients through transcriptome-wide association studies (TWAS) and summary-data-based Mendelian randomization (SMR) analysis. Methods: TWAS was performed by integrating the larger GWAS summary-data for OA (n=30,727 cases, n=297,191 controls) and 2 expression weight sets (muscle-skeletal tissue and whole blood). Colocalization analysis, conditional analysis, and fine-mapping analysis were also conducted. A broad description of the identified associations was obtained. In addition, a causal relationship between certain risk genes and OA was identified with SMR. Results: New significant genome-wide associations were found, including on chromosome 1q36.12 (rs1555024, P=4.24E-07) near the Conclusions: We revealed some novel OA-associated genes and risk loci by integrating multiple data types and analysis methods, thus providing new clues for the study of genetic mechanisms of OA.
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