The role of mitochondrial autophagy in osteoarthritis
Genchun Wang,
Xiong Zhang,
Jingting Xu,
Liangcai Hou,
Zhou Guo,
Kai Sun,
Fengjing Guo
Affiliations
Genchun Wang
Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; Orthopedic Medical Center, Union Hospital, Fujian Medical University, Fuzhou, Fujian 350000, China
Xiong Zhang
Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China
Jingting Xu
Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China
Liangcai Hou
Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China
Zhou Guo
Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China
Kai Sun
Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; Corresponding author
Fengjing Guo
Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; Corresponding author
Summary: Osteoarthritis (OA) is a progressive degenerative joint disease, and the underlying molecular mechanisms of OA remain poorly understood. This study aimed to elucidate the relationship between mitochondrial autophagy and OA by identifying key regulatory genes and their biological functions. Utilizing bioinformatics analyses of RNA expression profiles from the GSE55235 dataset, we identified 2,136 differentially expressed genes, leading to the discovery of hub genes associated with mitochondrial autophagy and OA. Gene set enrichment analysis (GSEA) revealed their involvement in critical pathways, highlighting their potential roles in OA pathogenesis. Furthermore, our study explored the immunological landscape of OA, identifying distinct immune cell infiltration patterns that contribute to the disease’s inflammatory profile. We also evaluated the therapeutic potential of drugs targeting these hub genes, suggesting potential approaches for OA treatment. Collectively, this study advances our knowledge of mitochondrial autophagy in OA and proposes promising biomarkers and therapeutic targets.