Besides, enrichment analysis of 1017 significantly down-regulated genes in Figure 4C,D implied that the lesion site of skeletal muscle damage after stroke was primarily the mitochondria (mitochondrial inner membrane; mitochondrial respiratory chain complex I; mitochondrion; mitochondrial respiratory chain complex IV) and that the pathological process may be associated with a decline in mitochondrial function (mitochondrial respiratory chain complex I assembly; mitochondrial electron transport, NADH to ubiquinone; NADH dehydrogenase (ubiquinone) activity; cytochrome-c oxidase activity). This evidence concerns the gene NDUFV1 and stroke disorder.