AbstractSpinal cord injury (SCI) is often accompanied by muscle atrophy; however, its underlying mechanisms remain unclear. Here, the molecular mechanisms of muscle atrophy following SCI were investigated. The GSE45550 gene expression profile of control (before SCI) and experimental (14 days following SCI) groups, consisting of Sprague–Dawley rat soleus muscle (n = 6 per group), was downloaded from the Gene Expression Omnibus database, and then differentially expressed gene (DEG) identification and Gene Ontology, pathway, pathway network, and gene signal network analyses were performed. A total of 925 differentially expressed genes, 149 biological processes, and 55 pathways were screened. In the pathway network analysis, the 10 most important pathways were citrate cycle (TCA cycle), pyruvate metabolism, MAPK signalling pathway, fatty acid degradation, propanoate metabolism, apoptosis, focal adhesion, synthesis and degradation of ketone bodies, Wnt signalling, and cancer pathways. In the gene signal network analysis, the 10 most important genes were Acat1, Acadvl, Acaa2, Hadhb, Acss1, Oxct1, Hadha, Hadh, Acaca, and Cpt1b. Thus, we screened the key genes and pathways that may be involved in muscle atrophy after SCI and provided support for finding valuable markers for this disease.
Identification of critical genes associated with spinal cord injury based on the gene expression profile of spinal cord tissues from trkB.T1 knockout mice
