Pathophysiological mechanisms of diabetic cardiomyopathy and the therapeutic potential of epigallocatechin-3-gallate.

Cardiovascular complications are considered one of the leading causes of morbidity and mortality among diabetic patients. Diabetic cardiomyopathy (DCM) is a type of cardiovascular damage presents in diabetic patients independent of the coexistence of ischemic heart disease or hypertension. It is characterized by impaired diastolic relaxation time, myocardial dilatation and hypertrophy and reduced systolic and diastolic functions of the left ventricle. Molecular mechanisms underlying these pathological changes in the diabetic heart are most likely multifactorial and include, but not limited to, oxidative/nitrosative stress, increased advanced glycation end products, mitochondrial dysfunction, inflammation and cell death. The aim of this review is to address the major molecular mechanisms implicated in the pathogenesis of DCM. In addition, this review provides studies conducted to determine the pharmacological effects of (-)-epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, focusing on its therapeutic potential against the processes involved in the pathogenesis and progression of DCM. EGCG has been shown to exert several potential therapeutic properties both in vitro and in vivo. Given its therapeutic potential, EGCG might be a promising drug candidate to decrease the morbidity and mortality associated with DCM and other diabetes complications.