Denervation often results in skeletal muscle atrophy.Different mechanisms seem to be involved in the determination between denervated slow and fast skeletal muscle atrophy.At the epigenetic level,mi RNAs are thought to be highly involved in the pathophysiological progress of denervated muscles.We used mi RNA microarrays to determine mi RNA expression profiles from a typical slow muscle(soleus muscle) and a typical fast muscle(tibialis anterior muscle) at an early denervation stage in a rat model.Results showed that mi R-206,mi R-195,mi R-23 a,and mi R-30 e might be key factors in the transformation process from slow to fast muscle in denervated slow muscles.Additionally,certain mi RNA molecules(mi R-214,mi R-221,mi R-222,mi R-152,mi R-320,and Let-7e) could be key regulatory factors in the denervated atrophy process involved in fast muscle.Analysis of signaling pathway networks revealed the mi RNA molecules that were responsible for regulating certain signaling pathways,which were the final targets(e.g.,p38 MAPK pathway; Pax3/Pax7 regulates Utrophin and follistatin by HDAC4; IGF1/PI3K/Akt/m TOR pathway regulates atrogin-1 and Mu RF1 expression via Fox O phosphorylation).Our results provide a better understanding of the mechanisms of denervated skeletal muscle pathophysiology. Denervation often results in skeletal muscle atrophy. Different mechanisms seem to be involved in the determination between denervated slow and fast skeletal muscle atrophy. At the epigenetic level, miRNAs are thought to be highly involved in the pathophysiological progress of denervated muscles. RNA microarrays to determine mi RNA expression profiles from a typical slow muscle (soleus muscle) and a typical fast muscle (tibialis anterior muscle) at an early denervation stage in a rat model. Results showed that mi R-206, mi R-195, mi R-23 a, and mi R-30 e might be key factors in the transformation process from slow to fast muscle in denervated slow muscles. Additionally, certain miRNA molecules (mi R-214, mi R-221, mi R- 222, mi R-152, mi R-320, and Let-7e) could be key regulatory factors in the denervated atrophy process involved in fast muscle. Analysis of signaling pathway networks revealed the mi RNA molecules that were responsible for controlling certain signaling pathways , which were the f inal targets (eg, p38 MAPK pathway; Pax3 / Pax7 regulates Utrophin and follistatin by HDAC4; IGF1 / PI3K / Akt / m TOR pathway regulates atrogin-1 and Mu RF1 expression via Fox O phosphorylation) .Our results provide a better understanding of the mechanisms of denervated skeletal muscle pathophysiology.