Duchenne muscular dystrophy (DMD) is the most common and severe form of progressive muscular dystrophy, with an incidence of 1 to 3500–6000 live births. In patients with DMD, the problem of cardiovascular disorders is relevant, because the damage to the heart muscle and the cardiac conduction system is a factor that worsens prognoses. Long and short non-coding RNAs are differentially expressed in DMD and have a mechanism of action through targeted mRNAs. A subset of muscle-enriched miRNAs, the so-called myomiRs (miR-133, miR-206, miR-208), are grown in the serum of patients with DMD and in animal models with dystrophin deficiency, which may present an important biomarker. Purpose: to estimate the role of miR133a-3p, mir133b-3p, miR206-3p, miR208a3p, miR208b-3p in the development of cardiomyopathy in children with DMD. Material and methods: the retrospective study included 20 patients with confirmed molecular-genetic diagnoses of DMD and 9 patients in the control group. The anamnesis and clinical-paraclinical investigations, such as blood biochemistry (ALAT, ASAT, LDH, CK, CK-MB), EAB, electrocardiogram, echocardiography plus color Doppler were performed in the cardiology unit of the PMHI Mother and Child Care Institute. The extraction and analysis of the above-mentioned miRNA using the qPCR and RT methods were performed in the Genetic Center of Excellence PMHI Mother and Child Care Institute. Results: for the first time in the Genetic Center of Excellence, quantitative miRNA extraction was obtained. The protocol and study results will be presented at the congress. Conclusions: additional scientific evidence shows that nRNAs also play a role in dystrophin expression; In this way, their modulations could represent a potential therapeutic strategy to increase dystrophin levels in combination with other gene therapies.