Myocardial ischemic injury results from severe impairment of the coronary blood supply and may lead to metabolic and ultrastructural changes, thereby causing irreversible damage. MicroRNA (miR)‑20b‑5p has been demonstrated to be involved in malignancies of the breast, colorectum, stomach, blood and oropharynx. The present study aimed to investigate the effects of miR‑20b‑5p on ventricular remodeling following myocardial ischemia‑reperfusion (IR) injury in rats by targeting small mothers against decapentaplegic homolog 7 (Smad7) via the transforming growth factor‑β (TGF‑β)/Smad signaling pathway. A total of 70 adult male Sprague‑Dawley rats were divided into seven groups: Sham group, IR group, negative control group, miR‑20b‑5p mimics group, miR‑20b‑5p inhibitors group, small interfering RNA (siRNA)‑Smad7 group, and miR‑20b‑5p inhibitors + siRNA‑Smad7 group. Dual luciferase reporter gene assays were used to verify the association between miR‑20b‑5p and Smad7. Myocardial infarction size, myocardial collagen volume fraction and perivascular collagen area were detected separately using triphenyltetrazolium chloride and Masson's staining. The rate of positive expression of Smad7 was detected using immunohistochemistry, and the expression levels of miR‑20b‑5p, TGF‑β1, Smad3 and Smad7 were detected using reverse transcription‑quantitative polymerase chain reaction and western blot analyses. The findings revealed that miR‑20b‑5p inhibited Smad7. Compared with the sham group, the other six groups had increased myocardial infarction size, myocardial collagen, and expression of miR‑20b‑5p, TGF‑β1 and Smad3, and decreased expression of Smad7. Compared with the IR group, the miR‑20b‑5p mimics group and the siRNA‑Smad7 group had increased myocardial infarction size and myocardial collagen, increased expression of TGF‑β1 and Smad3, and decreased expression of Smad7. The expression of miR‑20b‑5p was markedly increased in the miR‑20b‑5p mimics group, but did not differ significantly from that in the siRNA‑Smad7 group. The results demonstrated that miR‑20b‑5p promoted ventricular remodeling following myocardial IR injury in rats by inhibiting the expression of Smad7 through activating the TGF‑β/Smad signaling pathway.