Tribbles同源蛋白3参与糖尿病性心肌病的机制探讨

糖尿病可以独立于高血压、心脏瓣膜疾病、冠心病等其他心脏病因素之外,导致心脏结构和功能的异常,引起糖尿病性心肌病。Tribbles同源蛋白3是肥胖、糖尿病和动脉粥样硬化等代谢性疾病的关键性枢纽蛋白,可以通过胰岛素抵抗、内质网应激、脂质代谢等一系列途径,促使糖尿病并发症的形成。     

硫化氢对糖尿病心肌病的保护作用

糖尿病心肌病是指发生于糖尿病患者,不能用高血压性心脏病、冠状动脉粥样硬化性心脏病及其他心脏病变来解释的一种特异性心肌病。研究表明,硫化氢作为内源性气体信号分子,对糖尿病心肌病心脏具有保护作用,其机制主要与减轻炎症反应,减轻氧化应激损伤,抑制心肌细胞凋亡,促进自噬有关。     

促红细胞生成素对糖尿病心肌病保护作用的研究进展

糖尿病心肌病是指发生于糖尿病患者,有心脏结构和功能的改变,而不能用高血压性心脏病、冠心病、心脏瓣膜病及其他心脏病变来解释的一种心肌疾病。目前有许多关于糖尿病心肌病的作用机制及治疗方面的研究。现主要对糖尿病心肌病作用机制及促红细胞生成素对糖尿病心肌病的保护作用做一综述。     

糖尿病心肌病与糠尿病心脏病是一回事吗？

糖尿病心肌病属于微血管病变 糖尿病性心脏病是指由于糖尿病所引起的,在糖和脂肪等多种代谢紊乱长期得不到纠正的基础上,在心脏所发生的大血管病变、微血管病变以及自主神经病变。其中大血管主要是位于心脏表面的冠状动脉,即所谓的糖尿病合并冠心病;     

糖尿病心肌病的研究进展

糖尿病心肌病的研究进展解放军第３０９医院（北京，１０００９１）刘振平解放军总医院（北京，１００８５３）田慧糖尿病心脏病的４个主要因素是冠状动脉疾病、糖尿病自主神经性心脏病、糖尿病心肌病和糖尿病心脏毛细血管病变。与年龄、性别匹配的正常对照相比，糖尿病（...     

离子通道在糖尿病心肌病中研究新进展

糖尿病性心肌病（diabetes cardiomyopathy,DCM）是继发于糖尿病的一种特异性心肌病,其独立于高血压性、冠状动脉粥样硬化性或其他原因所致心脏病。DCM以心肌代谢紊乱和心脏微血管病变为基础,导致广泛的局灶性心肌坏死,随后发展为收缩功能障碍,最终表现为心力衰竭。离子通道在维持心肌细胞膜电位、信号传导、心肌细胞代谢方面发挥着重要作用,近年来的研究发现,钙、钾、钠等阳离子通道以及阴离子通道的改变是糖尿病心肌病发病的重要基础。本文从离子通道这一视角出发,系统性综述了糖尿病心肌病研究新进展。     

糖尿病心脏病的中西医治疗

糖尿病性心脏病是指糖尿病患者所并发或伴发的心脏病。包括糖尿病性心脏病、大血管病变(冠心病)、糖尿病性心肌病、糖尿病性微血管病变和糖尿病性心脏自主神经病变引发的心率、心律和心功能异常，以及糖尿病性高血压所并发的高血压心脏病。     

糖尿病性心脏病的中西医结合防治

糖尿病性心脏病，包括了糖尿病冠状动脉粥样硬化性心脏病、糖尿病性心肌病和糖尿病性心脏植物神经病变。研究表明，因糖尿病性心脏病而死亡的患者约占糖尿病患者病死率的80％，其中约70％是死于冠心病。     

糖友，你的心脏还好吗？

糖尿病最重要的并发症之一是心血管系统病变,该并发症已成为糖尿病患者健康和劳动力的严重威胁,是造成死亡的主要原因。糖尿病心脏病主要包括：糖尿病心脏微血管病变、大血管病变、心肌病变和心脏自主神经功能紊乱等。那么我们应该如何保护心脏呢？     

过氧化物酶体增殖物激活受体α与糖尿病心肌病

糖尿病心肌病是常见的糖尿病慢性并发症 ,目前认为能量代谢紊乱在糖尿病心肌病的发病中起重要作用。过氧化物酶体增殖物激活受体α(PPAR α)是一种配体活化型转录因子 ,其主要的生理作用为调节脂肪酸的氧化代谢。在糖尿病个体的心肌细胞中 ,PPAR α表达水平上调 ,由此引起心肌细胞糖脂代谢紊乱 ,最终导致心肌细胞受损、心脏收缩、舒张功能异常及糖尿病心肌病的发生。     

Diabetic cardiomyopathy: evidence, mechanisms, and therapeutic implications

The presence of a diabetic cardiomyopathy, independent of hypertension and coronary artery disease, is still controversial. This systematic review seeks to evaluate the evidence for the existence of this condition, to clarify the possible mechanisms responsible, and to consider possible therapeutic implications. The existence of a diabetic cardiomyopathy is supported by epidemiological findings showing the association of diabetes with heart failure; clinical studies confirming the association of diabetes with left ventricular dysfunction independent of hypertension, coronary artery disease, and other heart disease; and experimental evidence of myocardial structural and functional changes. The most important mechanisms of diabetic cardiomyopathy are metabolic disturbances (depletion of glucose transporter 4, increased free fatty acids, carnitine deficiency, changes in calcium homeostasis), myocardial fibrosis (association with increases in angiotensin II, IGF-I, and inflammatory cytokines), small vessel disease (microangiopathy, impaired coronary flow reserve, and endothelial dysfunction), cardiac autonomic neuropathy (denervation and alterations in myocardial catecholamine levels), and insulin resistance (hyperinsulinemia and reduced insulin sensitivity). This review presents evidence that diabetes is associated with a cardiomyopathy, independent of comorbid conditions, and that metabolic disturbances, myocardial fibrosis, small vessel disease, cardiac autonomic neuropathy, and insulin resistance may all contribute to the development of diabetic heart disease.     

Diabetic cardiomyopathy: a hyperglycaemia- and insulin-resistance-induced heart disease

Diabetic cardiomyopathy is characterised in its early stages by diastolic relaxation abnormalities and later by clinical heart failure in the absence of dyslipidaemia, hypertension and coronary artery disease. Insulin resistance, hyperinsulinaemia and hyperglycaemia are each independent risk factors for the development of diabetic cardiomyopathy. The pathophysiological factors in diabetes that drive the development of cardiomyopathy include systemic metabolic disorders, inappropriate activation of the renin–angiotensin–aldosterone system, subcellular component abnormalities, oxidative stress, inflammation and dysfunctional immune modulation. These abnormalities collectively promote cardiac tissue interstitial fibrosis, cardiac stiffness/diastolic dysfunction and, later, systolic dysfunction, precipitating the syndrome of clinical heart failure. Recent evidence has revealed that dysregulation of coronary endothelial cells and exosomes also contributes to the pathology behind diabetic cardiomyopathy. Herein, we review the relationships among insulin resistance/hyperinsulinaemia, hyperglycaemia and the development of cardiac dysfunction. We summarise the current understanding of the pathophysiological mechanisms in diabetic cardiomyopathy and explore potential preventative and therapeutic strategies.     

Diabetic cardiomyopathy: concept,heart function,and pathogenesis

The diabetic cardiomyopathy is a disease caused by diabetes and is characterised by the presence of diastolic and/or systolic left ventricular dysfunction. Diabetes may produce metabolic alterations, interstitial fibrosis, myocellular hypertrophy, microvascular disease and autonomic dysfunction. It is thought that all of them may cause cardiomyopathy. Other abnormalities that are usually associated with diabetes such as hypertension, coronary artery disease and nephropathy should be excluded before diagnosing diabetic cardiomyopathy. There is no evidence that diabetic cardiomyopathy alone can produce heart failure. However, subclinical ventricular dysfunction has been described in young asymptomatic diabetic patients without other diseases that could affect the cardiac muscle. In these cases we should consider that diabetes is the only cause of the myocardial disease. More studies are needed to know the natural history of diabetic cardiomyopathy.     

Oxidative stress and diabetic cardiomyopathy: a brief review

Diabetes is a serious public health problem. Improvements in the treatment of noncardiac complications from diabetes have resulted in heart disease becoming a leading cause of death in diabetic patients. Several cardiovascular pathological consequences of diabetes such as hypertension affect the heart to varying degrees. However, hyperglycemia, as an independent risk factor, directly causes cardiac damage and leads to diabetic cardiomyopathy. Diabetic cardiomyopathy can occur independent of vascular disease, although the mechanisms are largely unknown. Previous studies have paid little attention to the direct effects of hyperglycemia on cardiac myocytes, and most studies, especially in vitro, have mainly focused on the molecular mechanisms underlying pathogenic alterations in vascular smooth-muscle cells and endothelial cells. Thus, a comprehensive understanding of the mechanisms of diabetic cardiomyopathy is urgently needed to develop approaches for the prevention and treatment of diabetic cardiac complications. This review provides a survey of current understanding of diabetic cardiomyopathy. Current consensus is that hyperglycemia results in the production of reactive oxygen and nitrogen species, which leads to oxidative myocardial injury. Alterations in myocardial structure and function occur in the late stage of diabetes. These chronic alterations are believed to result from acute cardiac responses to suddenly increased glucose levels at the early stage of diabetes. Oxidative stress, induced by reactive oxygen and nitrogen species derived from hyperglycemia, causes abnormal gene expression, altered signal transduction, and the activation of pathways leading to programmed myocardial cell deaths. The resulting myocardial cell loss thus plays a critical role in the development of diabetic cardiomyopathy. Advances in the application of various strategies for targeting the prevention of hyperglycemia-induced oxidative myocardial injury may be fruitful.     

糖尿病性心肌病的发病机制及治疗方法研究进展

心血管疾病是2型糖尿病的主要并发症,约占2型糖尿病患者死亡人数的2/3。血糖异常、血脂异常、胰岛素抵抗、慢性低度炎症、氧化应激、内皮功能障碍、血管钙化和高凝状态等多种病理生理过程可加快2型糖尿病患者糖尿病心脏病的进展。糖尿病性心肌病是糖尿病心脏病中较为常见的一种,可导致心功能异常并最终进展为心力衰竭、心律失常,甚至猝死。本文综述了糖尿病性心肌病的发病机制,以及当前及未来潜在的治疗方法。     

Causes and characteristics of diabetic cardiomyopathy

Type 1 and type 2 diabetic patients are at increased risk of cardiomyopathy and heart failure is a major cause of death for these patients. Cardiomyopathy in diabetes is associated with a cluster of features including decreased diastolic compliance, interstitial fibrosis and myocyte hypertrophy. The mechanisms leading to diabetic cardiomyopathy remain uncertain. Diabetes is associated with most known risk factors for cardiac failure seen in the overall population, including obesity, dyslipidemia, thrombosis, infarction, hypertension, activation of multiple hormone and cytokine systems, autonomic neuropathy, endothelial dysfunction and coronary artery disease. In light of these common contributing pathologies it remains uncertain whether diabetic cardiomyopathy is a distinct disease. It is also uncertain which factors are most important to the overall incidence of heart failure in diabetic patients. This review focuses on factors that can have direct effects on diabetic cardiomyocytes: hyperglycemia, altered fuel use, and changes in the activity of insulin and angiotensin. Particular attention is given to the changes these factors can have on cardiac mitochondria and the role of reactive oxygen species in mediating injury to cardiomyocytes.     

Update on Diabetic Cardiomyopathy: Inches Forward,Miles to Go

Diabetes causes cardiomyopathy, both directly and by potentiating the effect of its common comorbidities, coronary artery disease and hypertension, on its development. With the common and growing prevalence of diabetes worldwide, diabetic cardiomyopathy is a significant public health problem. Recent research identifies both mitochondrial dysfunction and epigenetic effects as newly recognized factors in the complex pathogenesis of diabetic cardiomyopathy. Diagnostically, specialized echocardiography techniques, cardiac magnetic resonance imaging, and serologic biomarkers all appear to have promise in detecting the early stages of diabetic cardiomyopathy. Research into treatments includes both traditional diabetes and heart failure therapies, but also explores the potential of newer metabolic and anti-inflammatory agents. These recent insights provide important additions to our knowledge about diabetic cardiomyopathy, but much remains unknown.