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LncRNA PTS-1 Protects Against Osteoarthritis Through the miR-8085/E2F2 Axis.
J Inflamm Res
January 2025
Department of Orthopaedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, People's Republic of China.
Background: Osteoarthritis (OA) is a leading cause of pain, disability, and reduced mobility worldwide, characterized by metabolic imbalances in chondrocytes, extracellular matrix (ECM), and subchondral bone. Emerging evidence highlights the critical role of long non-coding RNAs (lncRNAs) in OA pathogenesis. This study focuses on lncRNA PTS-1, a novel lncRNA, to explore its function and regulatory mechanisms in OA progression.
View Article and Find Full Text PDFA vascularized microfluidic model of the osteochondral unit for modeling inflammatory response and therapeutic screening.
Lab Chip
December 2024
CFD Research Corporation, 6820 Moquin Dr. N.W., Huntsville, AL 35806, USA.
Osteoarthritis (OA) has long been considered a disease of the articular cartilage. Within the past decade it has become increasingly clear that OA is a disease of the entire joint space and that interactions between articular cartilage and subchondral bone likely play an important role in the disease. Driven by this knowledge, we have created a novel microphysiological model of the osteochondral unit containing synovium, cartilage, bone, and vasculature in separate compartments with molecular and direct cell-cell interaction between the cells from the different tissue types.
View Article and Find Full Text PDFTranscriptomic integration and ligand-receptor crosstalk reveal the underlying molecular mechanisms between hip cartilage and subchondral bone in osteonecrosis of femoral head.
Gene
March 2025
Department of Orthopedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province 710004, China. Electronic address:
Osteonecrosis of femoral head (ONFH) is characterized not only by ischemic bone tissue necrosis but also by cartilage degeneration, which plays an essential role in the pathogenesis of ONFH. The molecular communication between tissues contributes to disease progression, however the communication between cartilage and subchondral bone in the progression of ONFH remains unclear. In this study, we integrated transcriptomic data from ONFH cartilage and subchondral bone, exploring common differentially expressed genes (DEGs), pathway and function enrichment analyses, the protein-protein interaction (PPI) network, and hub genes to comprehensively study molecular integration.
View Article and Find Full Text PDFCleavage of Cartilage Oligomeric Matrix Protein (COMP) by ADAMTS4 generates a neoepitope associated with osteoarthritis and other forms of degenerative joint disease.
Matrix Biol
February 2025
Department of Immunology and Inflammation, Imperial College London, Du Cane Road, London W12 0NN, United Kingdom; Department of Biochemical Sciences, School of Biosciences, Faculty of Health and Medical Sciences, Edward Jenner Building, University of Surrey, Guildford, Surrey GU2 7XH, United Kingdom. Electronic address:
Osteoarthritis (OA) is a highly prevalent joint disease, affecting millions of people worldwide and characterized by degradation of articular cartilage, subchondral bone remodeling and low-grade inflammation, leading to pain, stiffness and disability. Cartilage Oligomeric Matrix Protein (COMP) is a major structural component of cartilage and its degradation has been proposed as a marker of OA severity/progression. Several proteases cleave COMP in vitro, however, it is unclear which of these COMPase activities is prevalent in an osteoarthritic joint.
View Article and Find Full Text PDFCross-talk of inflammation and cellular senescence: a new insight into the occurrence and progression of osteoarthritis.
Bone Res
December 2024
Department of Foot and Ankle Surgery, Beijing Tongren Hospital, Capital Medical University, 100730, Beijing, PR China.
Osteoarthritis (OA) poses a significant challenge in orthopedics. Inflammatory pathways are regarded as central mechanisms in the onset and progression of OA. Growing evidence suggests that senescence acts as a mediator in inflammation-induced OA.
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