Hyperglycemic memory in diabetic cardiomyopathy

doi:10.1007/s11684-021-0881-2

Front. Med.

2022, Vol. 16

Issue (1) : 25-38 https://doi.org/10.1007/s11684-021-0881-2

REVIEW

Hyperglycemic memory in diabetic cardiomyopathy

Jiabing Zhan, Chen Chen, Dao Wen Wang(

), Huaping Li(

)

Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan 430030, China

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Abstract

Cardiovascular diseases account for approximately 80% of deaths among individuals with diabetes mellitus, with diabetic cardiomyopathy as the major diabetic cardiovascular complication. Hyperglycemia is a symptom that abnormally activates multiple downstream pathways and contributes to cardiac hypertrophy, fibrosis, apoptosis, and other pathophysiological changes. Although glycemic control has long been at the center of diabetes therapy, multicenter randomized clinical studies have revealed that intensive glycemic control fails to reduce heart failure-associated hospitalization and mortality in patients with diabetes. This finding indicates that hyperglycemic stress persists in the cardiovascular system of patients with diabetes even if blood glucose level is tightly controlled to the normal level. This process is now referred to as hyperglycemic memory (HGM) phenomenon. We briefly reviewed herein the current advances that have been achieved in research on the underlying mechanisms of HGM in diabetic cardiomyopathy.

Keywords diabetes diabetic cardiomyopathy hyperglycemic memory

Corresponding Author(s): Dao Wen Wang,Huaping Li

Just Accepted Date: 29 November 2021 Online First Date: 17 December 2021 Issue Date: 28 March 2022

Cite this article:

Jiabing Zhan,Chen Chen,Dao Wen Wang, et al. Hyperglycemic memory in diabetic cardiomyopathy[J]. Front. Med., 2022, 16(1): 25-38.

URL:

https://academic.hep.com.cn/fmd/EN/10.1007/s11684-021-0881-2
https://academic.hep.com.cn/fmd/EN/Y2022/V16/I1/25

Fig.1 AGEs promote the process of diabetic cardiomyopathy via various pathways in multiple cell types.

Fig.2 Elevated miR-320 in the heart of diabetic mice acts in the nucleus to promote CD36 transcription by facilitating the association of argonaute 2 (Ago2) with RNA polymerase II, which increases the FFA uptake of cardiomyocytes and results in myocardial lipid deposition, causing cell apoptosis and cardiac dysfunction. Adapted from reference [37] with permission (OA related license).

Fig.3 Various pathogenic mechanisms by which diabetic cardiomyopathy (DCM) forms a complex network.

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