부산대학교 도서관

Objectives: Accumulating evidence indicates a strong link between knee osteoarthritis (KOA) and sarcopenia. However, the mechanisms involved have not yet been elucidated. This study primarily aims to explore the molecular mechanisms that explain the connection between these 2 disorders. Methods: The gene expression profiles for KOA and sarcopenia were obtained from the Gene Expression Omnibus database, specifically from GSE55235, GSE169077, and GSE1408. Various bioinformatics techniques were employed to identify and analyze common differentially expressed genes (DEGs) across the 3 datasets. The techniques involved the analysis of Gene Ontology and pathways to enhance understanding, examining proteinprotein interaction (PPI) networks, and identifying hub genes. In addition, we constructed the network of interactions between transcription factors (TFs) and genes, the co-regulatory network of TFs and miRNAs for hub genes, and predicted potential drugs. Results: In total, 14 common DEGs were found between KOA and sarcopenia. Detailed information on biological processes and signaling pathways of common DEGs was obtained through enrichment analysis. After performing PPI network analysis, we discovered 4 hub genes (FOXO3, BCL6, CDKN1A, and CEBPB). Subsequently, we developed coregulatory networks for these hub genes involving TF-gene and TF-miRNA interactions. Finally, we identified 10 potential chemical compounds. Conclusions: By conducting bioinformatics analysis, our study has successfully identified common gene interaction networks between KOA and sarcopenia. The potential of these findings to offer revolutionary understanding into the common development of these 2 conditions could lead to the identification of valuable targets for therapy. 1. Introduction Knee osteoarthritis (KOA) is a prevalent degenerative condition of the musculoskeletal system that predominantly impacts individuals in the middle-aged and older age groups. This progressive ailment gradually impairs the patient’s mobility and overall well-being [1,2]. The primary pathological feature of knee osteoarthritis (KOA) involves the breakdown and loss of articular cartilage. Different joint tissues are impacted to different extents, including remodeling of the subchondral bone, degeneration of the meniscus, weakening and looseness of ligaments, inflammation of the infrapatellar fat pad, and inflammation of the synovial membrane [2–5]. Furthermore, the presence of periarticular muscle atrophy plays a significant role in the progression of KOA. Decreased muscle strength can alter mechanical stress, reduce joint stability, and accelerate cartilage degeneration and abnormal subchondral bone changes [6–9]. Sarcopenia, which frequently coexists with KOA [10–12], is primarily characterized by the decline in both muscle mass and strengt