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糖尿病性心肌病的复杂性:来自患者和动物模型的经验教训。

The complexities of diabetic cardiomyopathy: lessons from patients and animal models.

作者信息

Harmancey Romain, Taegtmeyer Heinrich

机构信息

Department of Internal Medicine, Division of Cardiology, University of Texas Medical School at Houston, 6431 Fannin Street, MSB 1.246, Houston, TX 77030, USA.

出版信息

Curr Diab Rep. 2008 Jun;8(3):243-8. doi: 10.1007/s11892-008-0042-x.

DOI:10.1007/s11892-008-0042-x
PMID:18625124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3637972/
Abstract

Cardiovascular diseases are foreseeable complications of diabetes mellitus; heart failure is a prominent complication among these. Diabetic cardiomyopathy is a distinct entity independent of coronary artery disease and hypertension. Most of our knowledge on diabetic cardiomyopathy's pathogenesis comes from studies performed on various animal models. The recent advances in the domain confirm that the disease is above all a maladaptation of the heart mostly driven by the metabolic derangements that accompany diabetes mellitus.

摘要

心血管疾病是糖尿病可预见的并发症;心力衰竭是其中突出的并发症。糖尿病性心肌病是一种独立于冠状动脉疾病和高血压的独特病症。我们对糖尿病性心肌病发病机制的大部分了解来自于对各种动物模型进行的研究。该领域的最新进展证实,这种疾病首先是心脏的一种适应不良,主要由糖尿病伴随的代谢紊乱所驱动。

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本文引用的文献

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Intracardiac lipid accumulation, lipoatrophy of muscle cells and expansion of myocardial infarction in type 2 diabetic patients.2型糖尿病患者的心内脂质蓄积、肌细胞脂肪萎缩及心肌梗死面积扩大。
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Diabetic Cardiomyopathy in OVE26 Mice Shows Mitochondrial ROS Production and Divergence Between In Vivo and In Vitro Contractility.OVE26小鼠的糖尿病性心肌病表现出线粒体活性氧生成以及体内和体外收缩性的差异。
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Nuclear receptors PPARbeta/delta and PPARalpha direct distinct metabolic regulatory programs in the mouse heart.核受体PPARβ/δ和PPARα在小鼠心脏中指导不同的代谢调控程序。
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Oxidative stress triggers cardiac fibrosis in the heart of diabetic rats.氧化应激引发糖尿病大鼠心脏的心肌纤维化。
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