Duchenne muscular dystrophy (DMD) is an X-linked recessive genetic disorder 
caused by out of frame mutations in the dystrophin gene. The hallmark symptoms 
of the condition include progressive degeneration of skeletal muscle, 
cardiomyopathy, and respiratory dysfunction. The most recent advances in 
therapeutic strategies for the treatment of DMD involve exon skipping or 
administration of minidystrophin, but these strategies are not yet universally 
available, nor have they proven to be a definitive cure for all DMD patients. 
Early diagnosis and tracking of symptom progression of DMD usually relies on 
creatine kinase tests, evaluation of patient performance in various ambulatory 
assessments, and detection of dystrophin from muscle biopsies, which are 
invasive and painful for the patient. While the current research focuses 
primarily on restoring functional dystrophin, accurate and minimally invasive 
methods to detect and track both symptom progression and the success of early 
DMD treatments are not yet available. In recent years, several groups have 
identified miRNA signature changes in DMD tissue samples, and a number of 
promising studies consistently detected changes in circulating miRNAs in blood 
samples of DMD patients. These results could potentially lead to non-invasive 
detection methods, new molecular approaches to treating DMD symptoms, and new 
methods to monitor of the efficacy of the therapy. In this review, we focus on 
the role of circulating miRNAs in DMD and highlight their potential both as a 
biomarker in the early detection of disease and as a therapeutic target in the 
prevention and treatment of DMD symptoms.