Cartilage degradation is the hallmark of osteoarthritis (OA). The purpose of this study was to identify and validate differentially expressed genes (DEGs) in human articular cartilage that could serve as potential therapeutic targets for hip OA. We performed transcriptomic profiling in a discovery cohort (12 OA-free and 72 hip OA-affected cartilage) and identified 179 DEGs between OA-free and OA-affected cartilage after correcting for multiple testing (P < 2.97 × 10-6). Pathway and network analyses found eight hub genes to be associated with hip OA (ASPN, COL1A2, MXRA5, P3H1, PCOLCE, SDC1, SPARC, and TLR2), which were all confirmed using qPCR in a validation cohort (36 OA-free and 62 hip OA-affected cartilage) (P < 6.25 × 10-3). Our data showed that dysregulation of extracellular matrix formation and imbalance in the proportion of collagen chains may contribute to the development of hip OA, and SDC1 could be a promising potential therapeutic target. These findings provided a better understanding of the molecular mechanisms for hip OA and may assist in developing targeted treatment strategies.
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http://dx.doi.org/10.1093/hmg/ddae200 | DOI Listing |
Commun Biol
January 2025
Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang, China.
Osteoarthritis (OA) is a degenerative joint disease that affects the cartilage and surrounding tissues. The transcription factor Kruppel-like family factor 9 (KLF9) has been identified as a regulator of tumorigenesis. However, its role in OA is still not fully understood.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Orthopedic Surgery, 920th Hospital of Joint Logistics Support Force of PLA, Kunming, China.
Osteoarthritis (OA) is a degenerative bone disease characterized by the destruction of joint cartilage and synovial inflammation, involving intricate immune regulation processes. Disulfidptosis, a novel form of programmed cell death, has recently been identified; however, the effects and roles of disulfidptosis-related genes (DR-DEGs) in OA remain unclear. We obtained six OA datasets from the GEO database, using four as training sets and two as validation sets.
View Article and Find Full Text PDFJ Adv Res
January 2025
Department of Rehabilitation Medicine, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361003, China. Electronic address:
Objective: The aim of this study was to investigate the potential molecular mechanisms by which taurine protects against cartilage degeneration.
Methods: The anterior cruciate ligament transection (ACLT) surgery was used to construct an animal model of osteoarthritis (OA). Metabolomics was used to identify characteristic metabolites in osteoarthritic chondrocytes.
The combination of hip arthroscopy and periacetabular osteotomy (PAO) has been proven safe and effective for addressing symptoms in patients with developmental dysplasia of the hip (DDH). As not every patient with dysplasia will require a hip arthroscopy to obtain desired clinical improvement in the setting of periacetabular osteotomy, a challenge is identifying which patients require adjacent procedures (either via arthroscopic or open) to fully treat their hip pathology. Even though labral repair is the most reported arthroscopic procedure in cases of hip dysplasia, I would suggest that labral treatment is the least likely helpful component of hip arthroscopy in these cases.
View Article and Find Full Text PDFHum Mol Genet
January 2025
Human Genetics & Genomics, Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, 300 Prince Philip Drive, St. John's, Newfoundland & Labrador, A1B 3V6, Canada.
Cartilage degradation is the hallmark of osteoarthritis (OA). The purpose of this study was to identify and validate differentially expressed genes (DEGs) in human articular cartilage that could serve as potential therapeutic targets for hip OA. We performed transcriptomic profiling in a discovery cohort (12 OA-free and 72 hip OA-affected cartilage) and identified 179 DEGs between OA-free and OA-affected cartilage after correcting for multiple testing (P < 2.
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