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糖尿病心肌病(DCM)指由糖尿病引起的,不能用冠状动脉粥样硬化性心脏病、高血压心脏病、瓣膜性心脏病及其他心脏病变解释的心肌病变,其表现为舒张或收缩功能障碍,最终发展为心力衰竭,与糖尿病患者的高死亡率密切相关。DCM的发病机制复杂,尚缺少特异性治疗方法。沉默信息调节因子6(SIRT6)是新近发现的DCM的治疗靶点,其可广泛参与DNA修复、端粒维持、糖脂代谢、炎症反应等多种生理活动。本文主要综述了DCM的发病机制、治疗,并分析了SIRT6调控DCM的机制:减轻心肌纤维化和脂毒性、抗氧化应激和抗炎、调控线粒体功能,以期为DCM的治疗提供一定参考。 相似文献
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糖尿病心肌病(diabetic cardiomyopathy,DCM)是糖尿病常见并发症之一,其发病机制仍未完全阐明。RhoA/ROCK信号通路介导胰岛素抵抗、氧化应激、炎症、细胞凋亡、心肌纤维化、心脏舒缩功能等途径参与DCM发病,且ROCK抑制剂——法舒地尔在DCM中显示了一定治疗作用。本文就RhoA/ROCK信号通路在DCM发病机制中的研究进展作一综述。 相似文献
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钠-葡萄糖共转运蛋白2抑制剂(SGLT2i)是新型降糖药物,对糖尿病心肌病(DCM)有明确的治疗效果。心脏重构作为DCM普遍存在的特征表现,因表型和机制的复杂性引起广泛关注。该文介绍DCM心脏重构的表现以及SGLT2i对DCM心脏重构改善作用的潜在机制。 相似文献
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目的探讨线粒体氧化应激(MOS)在糖尿病心肌病(DCM)发生发展中的作用和α-硫辛酸(α-LA)保护机制。方法大鼠分为正常对照(NC)组,糖尿病(DM)组,糖尿病α-LA治疗组(α-LA组)。4、8、12周末测定大鼠心功能、心脏胶原含量、线粒体谷胱甘肽(GSH)、MDA含量和Mn-SOD的活性,镜下观察心脏病理改变。结果随病程延长,DM组大鼠心功能受损加重、胶原含量增加,病理改变加重,心肌线粒体Mn-SOD的活性和GSH的含量下降,MDA的含量明显上升;α-LA治疗后能够显著逆转糖尿病大鼠上述指标的变化。MDA与心脏胶原含量呈正相关。结论糖尿病大鼠MOS与DCM发生发展密切相关,α-LA通过升高心肌线粒体Mn-SOD活性和GSH的含量减弱MOS损伤保护DCM。 相似文献
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糖尿病心肌病(diabetic cardiomyopathy,DCM)定义为糖尿病患者在排除冠状动脉疾病、高血压或心脏瓣膜病的情况下发生的心脏功能障碍的心肌疾病。其是一种慢性疾病,有复杂的病理生理过程,在早期不易被察觉,而往往只在病变进展到心力衰竭时才得以被发现。糖尿病患者发生心力衰竭病死率高,但发病机制仍不明确,目前已初步认识到心肌脂毒性在DCM中的作用。因此,本文主要对近些年关于脂毒性在DCM发病机制中的作用作一综述。 相似文献
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糖尿病心肌病发病机理研究进展 总被引:3,自引:0,他引:3
糖尿病心肌病是糖尿病患者罹患的一种特异性心肌疾病,多种因素在其发生、发展过程中发挥重要作用。主要包括心肌细胞的糖代射、脂代谢与能量代谢异常,心肌细胞的凋亡、坏死和纤维化引起的心肌结构改变,心肌微血管出现的一系列病变等等。现就近年来对糖尿病心肌病发病机理的研究做一综述。 相似文献
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脂质代谢异常诱发心肌结构和功能紊乱,进而导致糖尿病心肌病(DCM)的形成,已成为当前DCM研究的热点。CD36是主要的脂质跨膜转运蛋白,参与调节心脏脂质代谢,在DCM导致心肌损伤的分子机制中具有关键作用。本文总结了CD36的结构及其在特定细胞类型中的作用,并进一步探讨CD36在DCM中的病理生理作用,以及CD36作为靶点的潜在药物治疗策略。 相似文献
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组织蛋白酶L在扩张型心肌病心肌中的表达及其意义 总被引:1,自引:0,他引:1
目的探讨溶酶体组织蛋白酶L在扩张型心肌病(DCM)心肌组织中的表达及其在DCM发病中的意义。方法终末期扩张型心肌病行心脏移植术的受体标本20例(心肌病组)及脑死亡3h内排除心脏疾患的心脏标本5例(对照组),通过免疫组化、Westernblotting和实时定量RTPCR等方法检测心肌组织组织蛋白酶L基因转录及蛋白表达水平,并对组织蛋白酶LmRNA表达水平的动态变化与射血分数进行相关性分析。结果心肌病组心肌中组织蛋白酶LmRNA及蛋白表达水平均明显高于对照组,两组比较,差异有高度统计学意义(P值均<0.01);DCM患者心肌组织蛋白酶LmRNA表达水平与射血分数呈显著负相关(r=-0.884,P<0.01)。结论组织蛋白酶L过度激活可能在扩张型心肌病的发病机制中起重要作用。 相似文献
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Schupp M Kintscher U Fielitz J Thomas J Pregla R Hetzer R Unger T Regitz-Zagrosek V 《European journal of heart failure》2006,8(3):290-294
BACKGROUND: The peroxisome proliferator-activated receptor alpha (PPARalpha) is a central regulator of myocardial fatty acid (FA) metabolism implicated in the pathogenesis of heart failure. AIMS: To characterize PPARalpha regulation in human dilated cardiomyopathy (DCM), we studied the expression of cardiac PPARalpha, cardiac carnitine palmitoyl-transferase I (CPT-1), a major PPARalpha target gene, and of the cardiac glucose transporter GLUT-4 in patients with DCM. METHODS: Left ventricular biopsies were taken from patients with DCM (n=16) and control subjects (n=15), and mRNA expression was quantitated using real-time PCR (SYBR((R))Green) and protein expression was measured by Western immunoblotting. RESULTS: Left ventricular PPARalpha mRNA levels were significantly increased in the DCM group compared to the control group (136+/-25.4% vs. control, p<0.01). Consistently, DCM patients had a significantly higher cardiac CPT-1 mRNA expression (147+/-51% vs. control, p<0.05) compared to the control group. Cardiac GLUT-4 expression was similar in both groups. CONCLUSION: Elevated cardiac PPARalpha levels followed by an induction of cardiac CPT-1 expression may result in increased fatty acid metabolism for cardiac energy production in DCM, suggesting a specific cardiac metabolic program in human DCM compared to other types of cardiomyopathy. 相似文献
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Hirooka K Yasumura Y Ishida Y Komamura K Hanatani A Nakatani S Yamagishi M Miyatake K 《Japanese circulation journal》2000,64(9):731-735
A 27-year-old man diagnosed as having dilated cardiomyopathy (DCM) without myocardial accumulation of 123I-beta-methyl-iodophenylpentadecanoic acid, and he was found to have type I CD36 deficiency. This abnormality of cardiac free fatty acid metabolism was also confirmed by other methods: 18F-fluoro-2-deoxyglucose positron emission tomography, measurements of myocardial respiratory quotient and cardiac fatty acid uptake. Although the type I CD36 deficiency was reconfirmed after 3 months, the abnormal free fatty acid metabolism improved after carvedilol therapy and was accompanied by improved cardiac function. Apart from a cause-and-effect relationship, carvedilol can improve cardiac function and increase free fatty acid metabolism in patients with both DCM and CD36 deficiency. 相似文献
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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。 相似文献
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Diabetes mellitus is characterized by fasting hyperglycaemia and the development of chronic vascular complications. While microvascular disease has been strongly related to glycaemic control, the major cause of mortality in diabetes is due to macrovascular disease affecting the cardiac and cerebrovascular circulations, which appear to have a more complex pathogenesis. Diabetes is associated with a 3–5-fold increase in death from myocardial infarction and similar figures pertain to stroke. The processes involved in atherothrombotic disease are complex and include variation in lipid metabolism, vascular responses, cell/cell interactions, and in the fluid and cellular phases of coagulation and fibrinolysis. The complex interactions between all of these processes are crucially altered by the metabolic milieu that characterizes diabetes mellitus, tipping the delicate balance towards atheroma formation, platelet aggregation and thrombus formation. This article will review these mechanisms and the effects of diabetes in the pathogenesis of vascular disease. © 1997 by John Wiley & Sons, Ltd. 相似文献
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摘要:目的探讨血清血管紧张素Ⅱ(angiotensin1I,Ang-Ⅱ)及转化生长因子α(transfomunggrowthfactorot,TGF-α)浓度在糖尿病(diabetesmellitus,DM)心肌病(diabeticcardiomyopathy.DCM)发病机制中的作用..方法检测118例DCM患者、40例单纯2型DM患者及50名健康体检者(正常对照组)的血清Ang-Ⅱ及TGF-α浓度,并进行对比分析。DCM患者按心功能分级(纽约心脏学会标准)分为3个亚组:35例心功能正常者设为DCMI组,42例心功能Ⅱ级者设为DCM2组,41例心功能Ⅲ-IV级者设为DCM3组。DCM组及DM组血清Ang-Ⅱ及TGF-仪浓度进行直线相关分析。结果血清Ang-Ⅱ及TGF-α的浓度在DCM各亚组[Ang-Ⅱ:(99.6_+20.3)、(116.9±26.5)、(137.5±33.7)pg/mL;TGF-α:(62.6±9.8)、(75.3±11.2)、(89.3±13.6)pg/mL]及DM组[Ang-1I:(83.9±17.1)pg/mL;TGF-α:(48.5±8.4)pg/mL]均显著高于正常对照组[Ang-U:(56.2±14.4)pg/mL;TGF-α:(26.8±5.1)pg/mL],差异有统计学意义(P均〈0.05)。DCM各亚组血清Ang-Ⅱ及TGF-α的浓度均屁著高于DM组.差异有统计学意义(P均〈0.05)。DCM组及DM组血清Ang-11与TGF-仪浓度呈正相关(r=0.93,P〈0.05;r=0.90.P〈0.05)。结论血清Ang-Ⅱ及TGF-仅浓度的升高,激活肾素血管紧张素系统,导致心肌纤维化可能是DCM的发病机制之一。 相似文献