The major findings of our study were that in vivo, BRD7 protein levels were increased in the cardiomyocytes of type 1 diabetic rats, and inhibition of BRD7 prevented diabetes‐induced myocardial remodelling and fibrosis, improved cardiac dysfunction and limited myocardial apoptosis; in vitro, HG increased the expression of BRD7 by HG‐induced phosphorylation of ERK1/2; moreover, BRD7 mediated HG‐induced apoptosis through ER stress pathway. The gene discussed is BRD7; the disease is type 1 diabetes mellitus.