索引超出了数组界限。 文章摘要
|本期目录/Table of Contents|

[1]赵,航,冯景辉,等.糖尿病心肌病发病机制的研究进展[J].国际心血管病杂志,2016,01:16-18.
点击复制

糖尿病心肌病发病机制的研究进展(PDF)

《国际心血管病杂志》[ISSN:1006-6977/CN:61-1281/TN]

期数:
2016年01期
页码:
16-18
栏目:
综述
出版日期:
2016-01-20

文章信息/Info

Title:
-
作者:
冯景辉吴秀萍
哈尔滨医科大学附属第一医院老年病科
Author(s):
-
关键词:
糖尿病心肌病发病机制心肌代谢活性氧
Keywords:
-
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2016.01.005
文献标识码:
-
摘要:
糖尿病心肌病是一种特异性心肌病,在一定程度上增加了糖尿病患者心力衰竭的发病风险。糖尿病心肌病的发病机制十分复杂,涉及多个方面,包括心肌代谢障碍、氧化应激、钙调节异常、线粒体解偶联等。该文主要介绍糖尿病心肌病发病机制的研究进展。
Abstract:
-

参考文献/References

[1] Huynh K, Kiriazis H, Du XJ, et al. Coenzyme Q10 attenuates diastolic dysfunction, cardiomyocyte hypertrophy and cardiac fibrosis in the db/db mouse model of type 2 diabetes[J]. Diabetologia, 2012, 55(5): 1544-1553.
[2] Ritchie RH, Love JE, Huynh K, et al. Enhanced phosphoinositide 3-kinase(p110α)activity prevents diabetes-induced cardiomyopathy and superoxide generation in a mouse model of diabetes[J]. Diabetologia, 2012, 55(12): 3369-3381.
[3] Glatz JF, Luiken JJ, Bonen A. Membrane fatty acid transporters as regulators of lipid metabolism: implications for metabolic disease[J]. Physiol Rev, 2010, 90(1): 367-417.
[4] Koonen DP, Febbraio M, Bonnet S, et al. CD36 expression contributes to age-induced cardiomyopathy in mice[J]. Circulation, 2007, 116(19): 2139-2147.
[5] Sung MM, Koonen DP, Soltys CL, et al. Increased CD36 expression in middle-aged mice contributes to obesity-related cardiac hypertrophy in the absence of cardiac dysfunction[J]. J Mol Med, 2011, 89(5): 459-469.
[6] Geloen A, Helin L, Geeraert B, et al. CD36 inhibitors reduce postprandial hypertriglyceridemia and protect against diabetic dyslipidemia and atherosclerosis[J]. PLoS One, 2012, 7(5): e37633-e37633.
[7] Brindley DN, Kok BP, Kienesberger PC, et al. Shedding light on the enigma of myocardial lipotoxicity: the involvement of known and putative regulators of fatty acid storage and mobilization[J]. Am J Physiol Endocrinol Metab, 2010, 298(5): E897-E908.
[8] Ussher JR, Folmes CD, Keung W, et al. Inhibition of serine palmitoyl transferase I reduces cardiac ceramide levels and increases glycolysis rates following diet-induced insulin resistance[J]. PLoS One, 2012, 7(5): e37703- e37703.
[9] 王庸晋, 刘 畅, 曹文君,等. 糖毒性对心肌细胞损伤的研究初探[J].国际心血管杂志, 2015, 42(3): 183-185.
[10] Kaludercic N, Carpi A, Nagayama T, et al. Monoamine oxidase B prompts mitochondrial and cardiac dysfunction in pressure overloaded hearts[J]. Antioxid Redox Signal, 2014, 20(2): 267-280.
[11] Kaludercic N, Takimoto E, Nagayama T, et al. Monoamine oxidase A–mediated enhanced catabolism of norepinephrine contributes to adverse remodeling and pump failure in hearts with pressure overload[J]. Circ Res, 2010, 106(1): 193-202.
[12] Aon MA, Cortassa S, O'Rourke B. Redox-optimized ROS balance: a unifying hypothesis[J]. Biochim Biophys Acta, 2010, 1797(6-7): 865-877.
[13] Cortassa S, O'Rourke B, Aon MA. Redox-optimized ROS balance and the relationship between mitochondrial respiration and ROS[J]. Biochim Biophys Acta, 2014, 1837(2): 287-295.
[14] Faria AM, Papadimitriou A, Silva KC, et al. Uncoupling endothelial nitric oxide synthase is ameliorated by green tea in experimental diabetes by re-establishing tetrahydrobiopterin levels[J]. Diabetes, 2012, 61(7): 1838-1847.
[15] Sivitz WI, Yorek MA. Mitochondrial dysfunction in diabetes: from molecular mechanisms to functional significance and therapeutic opportunities[J]. Antioxid Redox Signal, 2010, 12(4): 537-577.
[16] Williamson CL, Dabkowski ER, Baseler WA, et al. Enhanced apoptotic propensity in diabetic cardiac mitochondria: influence of subcellular spatial location[J]. Am J Physiol Heart Circ Physiol, 2010, 298(2): H633-H642.
[17] Piot C, Croisille P, Staat P, et al. Effect of cyclosporine on reperfusion injury in acute myocardial infarction[J]. N Engl J Med, 2008, 359(5): 473-481.
[18] Dong F, Zhang X, Yang X, et al. Impaired cardiac contractile function in ventricular myocytes from leptin-deficient ob/ob obese mice[J]. J Endocrinol, 2006, 188(1): 25-36.
[19] Dimitropoulos G, Tahrani AA, Stevens MJ. Cardiac autonomic neuropathy in patients with diabetes mellitus[J]. World J Diabetes, 2014, 5(1): 17-39.
[20] Tocchetti CG, Caceres V, Stanley BA, et al. GSH or palmitate preserves mitochondrial energetic/redox balance, preventing mechanical dysfunction in metabolically challenged myocytes/hearts from type 2 diabetic mice[J]. Diabetes, 2012, 61(12): 3094-3105.
[21] Duncan JG. Mitochondrial dysfunction in diabetic cardiomyopathy[J]. Biochim Biophys Acta, 2011, 1813(7): 1351-1359.
[22] Boudina S, Sena S, Theobald H, et al. Mitochondrial energetics in the heart in obesity-related diabetes direct evidence for increased uncoupled respiration and activation of uncoupling proteins[J]. Diabetes, 2007, 56(10): 2457-2466.
[23] Bugger H, Boudina S, Hu XX, et al. Type 1 diabetic akita mouse hearts are insulin sensitive but manifest structurally abnormal mitochondria that remain coupled despite increased uncoupling protein 3[J]. Diabetes, 2008, 57(11): 2924-2932.
[24] Turkieh A, Caubère C, Barutaut M, et al. Apolipoprotein O is mitochondrial and promotes lipotoxicity in heart[J]. J Clin Invest, 2014, 124(5): 2277-2286.

备注/Memo

备注/Memo:
基金项目:哈尔滨市科技创新人才研究专项资金项目(2012RFXXS050) 作者单位:哈尔滨医科大学附属第一医院老年病科 通信作者:吴秀萍,Email:Jenny0135@qq.com
更新日期/Last Update: 2016-01-20