Abstract
Diabetic cardiomyopathy refers to the heart disease without coronary artery disease and hypertension, diabetic patients with ventricular dysfunction. The molecular mechanism of diabetic cardiomyopathy remains unclear. Protein and lipid kinase phosphoinositol 3-kinase (PI3Ks) are thought to regulate cardiac damage in diabetes mellitus. This article reviews the role of PI3K subtypes and downstream signal transduction in the pathogenesis of diabetic cardiomyopathy, including cardiac metabolic regulation, contractility, hypertrophy, cardiomyocyte death and inflammation. Key words: 1-phosphatidylinositol 3-kinase; Diabetes complications; Cardiomyopathies/ET; Review
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