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Dafeng Yang [1] and Ya Wang [1] and Minna Jiang [1] and Xu Deng [2] and Zhifang Pei [1] and Fei Li [1] and Ke Xia [1] and Lingyan Zhu [3] and Tianlun Yang [1] and Meifang Chen [4]

Academic Editor: Shoichiro Ono

1, Department of Cardiology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China, csu.edu.cn

2, Department of Cardiology, Third Xiangya Hospital, Central South University, Changsha, Hunan 410006, China, csu.edu.cn

3, Department of Endocrinology, The First Affiliated Hospital of Nanchang University, Jiangxi 330006, China, ncu.edu.cn

4, Department of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China, csu.edu.cn

Received Jun 15, 2017; Revised Sep 8, 2017; Accepted Oct 4, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Cardiomyocytes hypertrophy and apoptosis is the crucial pathological foundation contributing to the onset and development of diabetic cardiomyopathy (DCM), which accounts for the major cause of disability and death among diabetic patients [1, 2]. Unfortunately, there is no efficient therapy to protect against DCM. Advanced glycation end products (AGEs), a group of heterogeneous compounds robustly formed under the condition of long high glucose, have been proven to be a pivotal driving force of the development and progression of DCM [3, 4]. Previous studies have demonstrated that the speed of AGEs accumulation in diabetic tissues, such as cardiomyocytes in heart failure, is much faster than in normal tissues [3, 5–7]. In addition, AGEs from the diet have also been proven to be an important factor promoting the progress of inflammation and oxidative stress [8, 9]. Recently, it was reported that binding of AGEs to their membrane receptor (receptor for AGEs, RAGE) increases the production of reactive oxygen species (ROS) and induces further production of AGEs, which subsequently promotes cardiomyocytes hypertrophy, apoptosis, and myocardial fibrosis, ultimately leading to heart failure [10–13]. More importantly, this process is prolonged and irreversible and this phenomenon is called “metabolic memory.” Therefore, the levels of AGEs are thought to be a new biomarker using as a diagnostic and prognostic tool to evaluate organ damage in diabetic patients [14, 15] and become an attractive pharmacologic target for...

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