BACKGROUND: Muscle atrophy is often associated with spinal cord injury, but its underlying mechanisms are still unclear. OBJECTIVE: To explore the molecular biological mechanism of muscle atrophy after spinal cord injury. METHODS: Gene profile GSE45550 for muscle atrophy after spinal cord injury in the gene expression database was analyzed. The gene expression profile GSE45550 included a control group (pre-spinal cord injury), an experimental group 1 (3 days after spinal cord injury), an experimental group 2 (8 days after spinal cord injury), and an experimental group 3 (14 days after spinal cord injury). The tissue was the soleus muscle of Sprague-Dawley rats (n=6/group). Four groups of sample data were then subjected to differential gene analysis, GO analysis, and pathway analysis. RESULTS AND CONCLUSION: Totally 2 513 differentially expressed genes were identified, of which Wnt16 Obfc1, Ufd1l, LOC100361067, Hhatl, Fxyd1, Psmc4, Tasp1, Mettl21c, and Ufd1l differential expressions were most significant. Biological processes such as biological process, G-protein coupled receptor signaling pathway, response to drug, transcription DNA-dependent, positive regulation of transcription DNA-dependent, oxidation-reduction process, ubiquitin-dependent protein catabolic process, apoptotic process, positive regulation of transcription from RNA polymeras, and fatty acid beta-oxidation, signaling pathways such as MAPK signaling, apoptosis, and citric acid cycle may play important roles. This study completely reveals the differentially expressed genes of muscle atrophy after spinal cord injury gene profiles, the involved biological processes, and signaling pathways. Wnt16 may be a key gene in muscle atrophy after spinal cord injury, providing molecular targets for future therapeutic progress. [ABSTRACT FROM AUTHOR]