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Dilated cardiomyopathy (DCM) is associated with sudden cardiac death and heart failure, resulting in a significant medical burden. The mechanisms underlying the pathogenesis of DCM remain elusive. In the present study, human cardiac tissues from patients with DCM and healthy donors were collected and their pathology was examined. The expression levels of apoptosis regulator Bcl-2 and fibrosis-associated microRNAs were also evaluated. Extensive myocardial fibrosis and apoptosis in DCM cardiac tissues was observed. As demonstrated by western blotting, reverse transcription-quantitative polymerase chain reaction and immunohistochemistry, the expression of Bcl‑2 was significantly increased in the apex, and the left and right ventricle of the heart in patients with DCM. In the specified locations, it was identified that miR‑21 was upregulated, while members of miR‑29 family (miR‑29a, miR‑29b and miR‑29c) and miR‑133 family (miR-133a and miR-133b) were downregulated. The present study suggested that Bcl‑2 and specific microRNAs may be involved in DCM pathogenesis, with a potential implication as therapeutic targets.

Expression of Bcl-2 and microRNAs in cardiac tissues of patients with dilated cardiomyopathy