Molecular mechanisms of diabetic cardiomyopathy.

Molecular mechanisms of diabetic cardiomyopathy.
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DOI:
10.1007/s00125-014-3171-6
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发表时间:
2014-04
期刊:
影响因子:
8.2
通讯作者:
Abel, E. Dale
Abel, E. Dale
中科院分区:
医学1区
文献类型:
--
作者:
Bugger, Heiko;Abel, E. Dale

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近年来,糖尿病已成为一种流行病,并且现在是最普遍的疾病之一。心血管并发症是糖尿病患者死亡和发病的主要原因。虽然缺血事件是糖尿病心脏并发症的主要原因,但人们普遍认为,在没有明显心肌缺血和高血压的情况下,发生心力衰竭的风险也会增加,或者在存在这些合并症的情况下会加速。这些与糖尿病相关的心肌结构和功能变化被称为糖尿病心肌病。在对1型或2型糖尿病的各种动物模型和转基因小鼠模型进行分析后,已经提出了许多有助于糖尿病心肌病发展的分子机制。关于这一主题的新机制数据的报告稳步增加,扩大了潜在的潜在机制列表。目前的审查提供了一个更新的分子改变,可能有助于在糖尿病心脏的结构和功能的改变。
In recent years, diabetes mellitus has become an epidemic and now represents one of the most prevalent disorders. Cardiovascular complications are the major cause of mortality and morbidity in diabetic patients. While ischaemic events dominate the cardiac complications of diabetes, it is widely recognised that the risk for developing heart failure is also increased in the absence of overt myocardial ischaemia and hypertension or is accelerated in the presence of these comorbidities. These diabetes-associated changes in myocardial structure and function have been called diabetic cardiomyopathy. Numerous molecular mechanisms have been proposed to contribute to the development of diabetic cardiomyopathy following analysis of various animal models of type 1 or type 2 diabetes and in genetically modified mouse models. The steady increase in reports presenting novel mechanistic data on this subject expands the list of potential underlying mechanisms. The current review provides an update on molecular alterations that may contribute to the structural and functional alterations in the diabetic heart.
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