Recent Advances in Epigenetics of Macrovascular Complications in Diabetes Mellitus

被引:19
|
作者
Pang, Mingchang [1 ]
Li, Yalan [2 ]
Gu, Wen [1 ]
Sun, Zhen [2 ]
Wang, Zhongqun [2 ]
Li, Lihua [1 ]
机构
[1] Jiangsu Univ, Dept Pathol, Affiliated Hosp, 438 Jiefang Rd North, Zhenjiang 212001, Jiangsu, Peoples R China
[2] Jiangsu Univ, Dept Cardiol, Affiliated Hosp, Zhenjiang, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Diabetes mellitus; Macrovascular complications; Atherosclerosis; Epigenetics; SMOOTH-MUSCLE-CELLS; DNA METHYLATION; ENDOTHELIAL DYSFUNCTION; MICROVASCULAR DYSFUNCTION; INSULIN-RESISTANCE; ATHEROSCLEROSIS; INFLAMMATION; EXPRESSION; PROMOTES; GENES;
D O I
10.1016/j.hlc.2020.07.015
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Diabetes mellitus is a metabolic and endocrine disorder characterised by hyperglycaemia. Type 2 diabetes mellitus accounts for >90% of people with diabetes. Disorders of blood glucose metabolism and a series of adverse reactions triggered by hyperglycaemia-such as oxidative stress and inflammation-are conducive to the occurrence of diabetic macrovascular complications, which pose severe challenges to the quality of life and life expectancy of people with diabetes. In recent years, epigenetics has attracted more and more researchers' attention as they explore the causes and treatment of diabetes. Epigenetics refers to the regulation of gene expression without changes in gene content. Research focusses on DNA methylation, histone post translational modification and non-coding RNA. A series of studies have shown that epigenetic regulation accelerates the development of atherosclerosis by interfering with the physiological activities of macrophages, endothelial cells and smooth muscle cells, such as inflammation, lipid deposition and apoptosis. Therefore, it is particularly important to explore new epigenetic discoveries to reduce the severity and harmfulness of diabetes. This study reviewed recent advances in epigenetics in the pathogenesis of diabetes mellitus and its macrovascular complications.
引用
收藏
页码:186 / 196
页数:11
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