Myocardial failure has a negative impact on the quality of human life. MicroRNA (miR) expression abnormalities lead to the development of many pathological conditions, including myocardial failure, and therefore the present study primarily focused on the investigation of the functions of miR-127 in the development of myocardial failure. The miR-127 expression levels in serum samples from patients with myocardial failure were examined. Oil red O staining was used to analyze the characteristics of the myocardium of the patients. Immunohistochemistry was used to detect fatty acid synthase (FASN), stearoyl-CoA desaturase-1 (SCD1) and mitochondrial brown fat uncoupling protein 1 (UCP1) protein expression in the myocardium of the patients. Furthermore, C57BL/6J (B6) mice were induced with 15 mg/kg of doxorubicin. Echocardiography was used to detect the histopathological alterations of the myocardial cells by comparison of the myocardial tissues from the myocardial failure animal model and normal C57BL/6 mice. Reverse transcription-quantitative polymerase chain reaction was used to detect the expression levels of miR-127 following different induction periods and immunohistochemistry was used to detect the expression of transforming growth factor-β1 (TGF-β1) and mothers against decapentaplegic homolog 3 (Smad3). Immunofluorescence was used to detect the expression alterations TGF-β1/Smad3 when miR-127 overexpression or inhibition was established. The results of the present study indicated that myocardial failure resulted in an upregulated expression of miR-127 and severe fat accumulation. FASN, SCD1 and UCP1 were highly expressed in the myocardial failure group compared with the control. Abdominal artery contraction and the ejection fraction were significantly reduced in the DOX-induced B6 mice. The cardiomyocytes became hypertrophic, and left ventricular systolic pressure and left ventricular maximum ejection pressure were altered following DOX induction in B6 mice. The results confirmed that miR-127 regulates the expression of TGF-β1/Smad3. The potential pathological mechanism of the effect of miR-127 may be based on the upregulation of the TGF-β1/Smad3 signaling pathway.

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