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糖尿病心肌病的分子机制。

Molecular mechanisms of diabetic cardiomyopathy.

机构信息

Cardiology and Angiology I, Heart Center Freiburg University, Freiburg, Germany.

出版信息

Diabetologia. 2014 Apr;57(4):660-71. doi: 10.1007/s00125-014-3171-6. Epub 2014 Jan 30.

DOI:10.1007/s00125-014-3171-6
PMID:24477973
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3969857/
Abstract

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.

摘要

近年来,糖尿病已成为一种流行病,现在是最常见的疾病之一。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,但人们普遍认识到,即使没有明显的心肌缺血、高血压或这些合并症存在,发生心力衰竭的风险也会增加。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。通过对 1 型和 2 型糖尿病的各种动物模型以及基因修饰的小鼠模型进行分析,提出了许多分子机制来解释糖尿病心肌病的发生。关于这个主题的新的机制数据的不断增加,扩展了潜在机制的清单。本综述提供了关于可能导致糖尿病心脏结构和功能改变的分子改变的最新信息。

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Diabetologia. 2014 Apr;57(4):660-71. doi: 10.1007/s00125-014-3171-6. Epub 2014 Jan 30.
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本文引用的文献

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Protein kinase RNA-like endoplasmic reticulum kinase (PERK) signaling pathway plays a major role in reactive oxygen species (ROS)-mediated endoplasmic reticulum stress-induced apoptosis in diabetic cardiomyopathy.蛋白激酶RNA样内质网激酶(PERK)信号通路在糖尿病性心肌病中由活性氧(ROS)介导的内质网应激诱导的细胞凋亡中起主要作用。
Cardiovasc Diabetol. 2013 Nov 2;12:158. doi: 10.1186/1475-2840-12-158.
2
Insulin receptor substrate signaling suppresses neonatal autophagy in the heart.胰岛素受体底物信号抑制心脏中的新生儿自噬。
J Clin Invest. 2013 Dec;123(12):5319-33. doi: 10.1172/JCI71171. Epub 2013 Nov 1.
3
Diabetic hyperglycaemia activates CaMKII and arrhythmias by O-linked glycosylation.
一种反映临床疾病进展的改良糖尿病性心肌病小鼠模型的深度表型分析。
Diabetol Metab Syndr. 2025 Aug 14;17(1):334. doi: 10.1186/s13098-025-01913-3.
4
Risk of Ischaemic and Non-Ischaemic Heart Failure in People With Type 2 Diabetes: Observational Study in 1.6 Million People in England.2型糖尿病患者发生缺血性和非缺血性心力衰竭的风险:对英国160万人的观察性研究。
Diabetes Metab Res Rev. 2025 Sep;41(6):e70072. doi: 10.1002/dmrr.70072.
5
UCP2 inhibition exaggerates diabetic cardiomyopathy by facilitating the activation of NLRP3 and pyroptosis.解偶联蛋白2(UCP2)抑制通过促进NLRP3激活和细胞焦亡加重糖尿病性心肌病。
Diabetol Metab Syndr. 2025 Jul 16;17(1):267. doi: 10.1186/s13098-025-01855-w.
6
From Type 2 Diabetes Mellitus To Diabetic Cardiomyopathy - A Systematic Review On The Role Of MicroRNA.从2型糖尿病到糖尿病性心肌病——关于微小RNA作用的系统综述
Curr Diab Rep. 2025 Jul 15;25(1):42. doi: 10.1007/s11892-025-01590-6.
7
High-Fat Diet-Induced Diabetic Cardiomyopathy in Female Zebrafish: Cardiac Pathology and Functional Decline Mediated by Type 2 Diabetes.高脂饮食诱导雌性斑马鱼糖尿病性心肌病:2型糖尿病介导的心脏病理及功能衰退
Nutrients. 2025 Jul 2;17(13):2209. doi: 10.3390/nu17132209.
8
Role of membrane microdomains in cardiac protection: strategies for diabetic cardiomyopathy.膜微区在心脏保护中的作用:糖尿病性心肌病的治疗策略
Am J Physiol Heart Circ Physiol. 2025 Aug 1;329(2):H572-H591. doi: 10.1152/ajpheart.00139.2025. Epub 2025 Jul 10.
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A Molecular Perspective on the Intricate Interplay Among Exosomes, Bioenergetic Metabolism, and the Pathogenesis of Diabetic Cardiomyopathy.关于外泌体、生物能量代谢与糖尿病性心肌病发病机制之间复杂相互作用的分子视角
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Beyond Heart Failure: Role of NT-Pro-BNP in Diabetes Mellitus Patients with Preserved Ejection Fraction.超越心力衰竭:N末端B型利钠肽原在射血分数保留的糖尿病患者中的作用
EJIFCC. 2025 Jun 3;36(2):165-170. eCollection 2025 Jun.
糖尿病高血糖通过 O-连接糖基化激活 CaMKII 并引发心律失常。
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Diabetes. 2013 Oct;62(10):3329-30. doi: 10.2337/db13-0683.
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Inducible overexpression of GLUT1 prevents mitochondrial dysfunction and attenuates structural remodeling in pressure overload but does not prevent left ventricular dysfunction.诱导型过表达 GLUT1 可预防压力超负荷引起的线粒体功能障碍和结构重构,但不能预防左心室功能障碍。
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Glucagon-like peptide-1 receptor activation reverses cardiac remodeling via normalizing cardiac steatosis and oxidative stress in type 2 diabetes.胰高血糖素样肽-1 受体激动剂通过纠正 2 型糖尿病心脏脂肪变性和氧化应激逆转心脏重构。
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J Diabetes Res. 2013;2013:630537. doi: 10.1155/2013/630537. Epub 2013 Mar 5.
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Free Radic Biol Med. 2013 Jul;60:307-17. doi: 10.1016/j.freeradbiomed.2013.02.021. Epub 2013 Feb 26.
10
The heme oxygenase system selectively enhances the anti-inflammatory macrophage-M2 phenotype, reduces pericardial adiposity, and ameliorated cardiac injury in diabetic cardiomyopathy in Zucker diabetic fatty rats.血红素加氧酶系统选择性增强抗炎型巨噬细胞-M2 表型,减少糖尿病性心肌病中 Zucker 肥胖型糖尿病大鼠的心包脂肪堆积,并改善心脏损伤。
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