Diabetic cardiomyopathy is one of the major complications of diabetes, and due 
to the increasing number of patients with diabetes it is a growing concern. 
Diabetes‑induced cardiomyopathy has a complex pathogenesis and histone 
deacetylase‑mediated epigenetic processes are of prominent importance. The 
olfactory bromodomain‑containing protein 4 (BRD4) is a protein that recognizes 
and binds acetylated lysine. It has been reported that the high expression of 
BRD4 is involved in the process of cardiac hypertrophy. The aim of the present 
study was to investigate the function of BRD4 in the process of high glucose 
(HG)‑induced cardiac hypertrophy, and to clarify whether epigenetic regulation 
involving BRD4 is an important mechanism. It was revealed that BRD4 expression 
levels were increased in H9C2 cells following 48 h of HG stimulation. This 
result was also observed in a diabetic rat model. Furthermore, HG stimulation 
resulted in the upregulation of the myocardial hypertrophy marker, atrial 
natriuretic peptide, the cytoskeletal protein α‑actin and fibrosis‑associated 
genes including transforming growth factor‑β, SMAD family member 3, connective 
tissue growth factor and collagen, type 1, α1. However, administration of the 
specific BRD4 inhibitor JQ1 (250 nM) for 48 h reversed this phenomenon. 
Furthermore, protein kinase B (AKT) phosphorylation was activated by HG 
stimulation and suppressed by JQ1. In conclusion, BRD4 serves an important role 
in the pathogenesis of HG‑induced cardiomyocyte hypertrophy through the AKT 
pathway.