CSF1 regulates inflammation and apoptosis in intervertebral disc degeneration

Intervertebral disc degeneration (IVDD) is a condition that severely impairs the quality of life for patients and is becoming increasingly prominent in aging societies. There is a pressing need to further investigate the mechanisms underlying the initiation and progression of IVDD. Current therapeutic approaches exhibit inconsistent efficacy, highlighting the urgency for the exploration of novel treatment strategies. In this study, we analyzed microarray datasets GSE147383 and GSE124272, downloaded from the Gene Expression Omnibus (GEO) database, which encompass 12 normal samples and 12 samples from patients with lumbar disc herniation. Utilizing R software, STRING, and various databases, we identified differentially expressed genes (DEGs) and constructed a protein-protein interaction (PPI) network. A total of 52 common DEGs were filtered from the datasets. The aim of this study was to investigate the effects of CSF1 knockdown on the inflammatory response and apoptosis in nucleus pulposus cells and to explore the relationship between peripheral blood CSF1 levels and IVDD. Employing cell culture and plasmid transfection techniques, along with the detection of inflammatory markers and analysis of cellular apoptosis, we found that CSF1 knockdown significantly reduced the expression levels of inflammation-related proteins in disc cells, indicating that CSF1 plays a crucial role in the regulation of inflammation and survival in disc cells. Serum testing from human sources also confirmed the significant role of CSF1 in the progression of IVDD. In summary, this study unravels the key role of CSF1 in intervertebral disc degeneration, providing a theoretical foundation for new treatment strategies and laying a solid foundation for future clinical applications. Future research should focus on the clinical application of CSF1 as a biomarker and its differential roles in various pathological states.