Abstract

Recent epidemiological and clinical studies have shown that type 2 diabetic patients can develop diabetic vascular complications even after intensive glycaemic control. It has been suggested that this phenomenon could be explained by the hypothesis of ‘metabolic memory’. The underlying mechanisms between these enduring effects and the prior hyperglycaemic state are still not well understood. Preliminary studies demonstrate that hyperglycaemia can regulate gene expression by epigenetic modifications, such as DNA methylation, which can persistently exist even after glucose normalization. Increasing evidence shows that epigenetic mechanisms may play a substantial role in the pathophysiology of diabetes and its associated vascular complications, including atherosclerosis, diabetic cardiomyopathy (DCM), nephropathy and retinopathy. In this review, we will examine the growing role of DNA methylation in diabetes and its vascular complications, thus it can provide critical implications for the early prevention of diabetes and its vascular complications.

Highlights

  • IntroductionThe epidemic of diabetes is a serious and growing public health problem. In 2015, the International Diabetes Federation (IDF) declared that 415 million people have diabetes and the number will rise to 642 million by 2040 worldwide [1]

  • Epidemiology of diabetes and its vascular complicationsThe epidemic of diabetes is a serious and growing public health problem

  • Diabetes is associated with significantly accelerated rates of several macrovascular complications such as atherosclerosis, diabetic cardiomyopathy (DCM) and other cardiovascular diseases and microvascular complications such as nephropathy and retinopathy [3,4]

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Summary

Introduction

The epidemic of diabetes is a serious and growing public health problem. In 2015, the International Diabetes Federation (IDF) declared that 415 million people have diabetes and the number will rise to 642 million by 2040 worldwide [1]. They activate multiple signal transduction pathways and regulate related gene expression, involving blood vessels, heart, kidney and eyes [17] It can increase the susceptibility of macrovascular complications such as atherosclerosis, DCM and microvascular complications such as nephropathy and retinopathy. In VSMCs, ECs and mouse models, altered DNA methylation of several candidate genes linked with atherosclerosis was identified, including vasodilator endothelial nitric oxide synthase, hypoxia-inducible c 2017 The Author(s) The aforementioned clinical studies, animal models and in vitro experiments have shown that DNA methylation may play a substantial role in the pathophysiology of diabetes and its associated vascular complications, including atherosclerosis, DCM, nephropathy and retinopathy. Hypoxia-inducible factor-1a, vasodilator endothelial nitric oxide synthase and matrix metalloproteinases

19 CpG sites
Conclusions
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