Abstract
Introduction: Osteoarthritis is a degenerative joint disease that leads to chronic pain, inflammation, and cartilage degradation, primarily affecting the elderly. The molecular mechanisms underlying osteoarthritis remain poorly understood, necessitating a comprehensive study of gene expression and protein interactions to identify key pathways and therapeutic targets.
Objectives: The primary objective of this study was to identify differentially expressed genes (DEGs) in synovial tissue of osteoarthritis patients and to analyze their associated protein-protein interaction (PPI) networks. By uncovering key regulatory genes, biological pathways, and potential drug targets, this research aims to enhance the understanding of osteoarthritis pathogenesis and contribute to the development of novel therapeutic strategies.
Materials and Methods: In this cross-sectional study, DEGs were identified from synovial tissue samples of osteoarthritis patients and healthy controls. Gene ontology (GO) and pathway enrichment analysis were performed, followed by PPI network construction to identify hub genes. Thirteen hub genes were identified from synovial tissue samples of osteoarthritis patients through differential expression and PPI network analysis. Further analysis included drug-target prediction using DrugBank database, transcription factor analysis via ENCODE, and promoter motif exploration using Tomtom and GOMO databases.
Results: Key pathways involved in osteoarthritis included PPAR signaling, lipolysis regulation, focal adhesion, and iron homeostasis. Drug-target analysis identified multiple candidates for pharmacological intervention, such as EGFR, TFRC, and LIPE. Promoter analysis revealed motifs linked to transcription factor activity, cytoskeletal organization, and inflammatory regulation, providing insight into upstream regulatory control.
Conclusion: This study highlights key genes and pathways involved in osteoarthritis, particularly those related to lipid metabolism, inflammation, and transcriptional regulation. The identified hub genes and their druggable potential offer promising avenues for developing targeted therapies to manage or slow disease progression.