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[1]Mozaffarian D,Benjamin EJ,Go AS,et al.Heart Disease and Stroke Statistics-2016 Update:A Report From the American Heart Association[J].Circulation,2016,133(4):e38-e360.
[2]Nguyen QM,Srinivasan SR,Xu JH,et al.Changes in risk variables of metabolic syndrome since childhood in pre-diabetic and type 2 diabetic subjects: the Bogalusa Heart Study[J].Diabetes care,2008,31(10):2044-2049.
[3]Aronson D,Edelman ER.Coronary Artery Disease and Diabetes Mellitus[J].Heart Fail Clin,2016,12(1):117-133.
[4]Suzuki H,Kayama Y,Sakamoto M,et al.Arachidonate 12/15-lipoxygenase-induced inflammation and oxidative stress are involved in the development of diabetic cardiomyopathy[J].Diabetes,2015,64(2):618-630.
[5]Anderson EJ,Kypson AP,Rodriguez E,et al.Substrate-specific derangements in mitochondrial metabolism and redox balance in the atrium of the type 2 diabetic human heart[J].J Am Coll Cardiol,2009,54(20):1891-1898.
[6]Raedschelders K,Ansley DM,Chen DD.The cellular and molecular origin of reactive oxygen species generation during myocardial ischemia and reperfusion Nov 10[J].Pharmacol Ther,2012,133(2):230-255.
[7]Wu Y,Xia ZY,Dou J,et al.Protective effect of ginsenoside Rb1 against myocardial ischemia/reperfusion injury in streptozotocin-induced diabetic rats[J].Mol Biol Rep,2011,38(7):4327-4335.
[8]Fiordaliso F,Leri A,Cesselli D,et al.Hyperglycemia activates p53 and p53-regulated genes leading to myocyte cell death[J].Diabetes,2001,50(10):2363-2375.
[9]Das A,Salloum FN,Filippone SM,et al.Inhibition of mammalian target of rapamycin protects against reperfusion injury in diabetic heart through STAT3 signaling[J].Basic Res Cardiol,2015,110(3):31.
[10]Gross ER,Hsu AK,Gross GJ.Diabetes abolishes morphine-induced cardioprotection via multiple pathways upstream of glycogen synthase kinase-3beta[J].Diabetes,2007,56(1):127-136.
[11]Ghaboura N,Tamareille S,Ducluzeau PH,et al.Diabetes mellitus abrogates erythropoietin-induced cardioprotection against ischemic-reperfusion injury by alteration of the RISK/GSK-3beta signaling[J].Basic Res Cardiol,2011,106(1):147-162.
[12]Drenger B,Ostrovsky IA,Barak M,et al.Diabetes blockade of sevoflurane postconditioning is not restored by insulin in the rat heart: phosphorylated signal transducer and activator of transcription 3- and phosphatidylinositol 3-kinase-mediated inhibition[J].Anesthesiology,2011,114(6):1364-1372.
[13]Zhuo C,Wang Y,Wang X,et al.Cardioprotection by ischemic postconditioning is abolished in depressed rats:role of Akt and signal transducer and activator of transcription-3[J].Mol Cell Biochem,2011,346(1-2):39-47.
[14]Ye J.Emerging role of adipose tissue hypoxia in obesity and insulin resistance[J].Int J Obes(Lond),2009,33(1):54-66.
[15]Sam F,Duhaney TA,Sato K,et al.Adiponectin deficiency,diastolic dysfunction,and diastolic heart failure[J].Endocrinology,2010,151(1):322-331.
[16]Rothenbacher D,Brenner H,Marz W,et al.Adiponectin,risk of coronary heart disease and correlations with cardiovascular risk markers[J].Eur Heart J,2005,26(16):1640-1646.
[17]Yi W,Sun Y,Gao E,et al.Reduced cardioprotective action of adiponectin in high-fat diet-induced type II diabetic mice and its underlying mechanisms[J].Antioxid Redox Signal,2011,15(7):1779-1788.
[18]Wang B,Raedschelders K,Shravah J,et al.Differences in myocardial PTEN expression and Akt signalling in type 2 diabetic and nondiabetic patients undergoing coronary bypass surgery[J].Clin Endocrinol(Oxf),2011,74(6):705-713.
[19]Aragno M,Mastrocola R,Alloatti G,et al.Oxidative stress triggers cardiac fibrosis in the heart of diabetic rats[J].Endocrinology,2008,149(1):380-388.
[20]Ghattas MH,Abo-Elmatty DM.Association of polymorphic markers of the catalase and superoxide dismutase genes with type 2 diabetes mellitus[J].DNA Cell Biol,2012,31(11):1598-1603.
[21]Lewis P,Stefanovic N,Pete J,et al.Lack of the antioxidant enzyme glutathione peroxidase-1 accelerates atherosclerosis in diabetic apolipoprotein E-deficient mice[J].Circulation,2007,115(16):2178-2187.
[22]Orasanu G,Plutzky J.The pathologic continuum of diabetic vascular disease[J].J Am Coll Cardiol,2009,53(5 Suppl):S35-S42.
[23]Yokota T,Kinugawa S,Hirabayashi K,et al.Oxidative stress in skeletal muscle impairs mitochondrial respiration and limits exercise capacity in type 2 diabetic mice[J].Am J Physiol Heart Circ Physiol,2009,297(3):H1069-H1077.
[24]Coudronniere N,Villalba M,Englund N,et al.NF-kappa B activation induced by T cell receptor/CD28 costimulation is mediated by protein kinase C-theta[J].Proc Natl Acad Sci USA,2000,97(7):3394-3399.
[25]Tang WH,Kravtsov GM,Sauert M,et al.Polyol pathway impairs the function of SERCA and RyR in ischemic-reperfused rat hearts by increasing oxidative modifications of these proteins[J].J Mol Cell Cardiol,2010,49(1):58-69.
[26]Forstermann U.Janus-faced role of endothelial NO synthase in vascular disease: uncoupling of oxygen reduction from NO synthesis and its pharmacological reversal[J].Biol Chem,2006,387(12):1521-1533.
[27]Chen CA,Wang TY,Varadharaj S,et al.S-glutathionylation uncouples eNOS and regulates its cellular and vascular function[J].Nature,2010,468(7327):1115-1118.
[28]Koka S,Das A,Salloum FN,et al.Phosphodiesterase-5 inhibitor tadalafil attenuates oxidative stress and protects against myocardial ischemia/reperfusion injury in type 2 diabetic mice[J].Free Radic Biol Med,2013,60:80-88.
[29]Yang JT,Qian LB,Zhang FJ,et al.Cardioprotective effects of luteolin on ischemia/reperfusion injury in diabetic rats are modulated by eNOS and the mitochondrial permeability transition pathway[J].J Cardiovasc Pharmacol,2015,65(4):349-356.
[30]Okazaki T,Otani H,Shimazu T,et al.Ascorbic acid and N-acetyl cysteine prevent uncoupling of nitric oxide synthase and increase tolerance to ischemia/reperfusion injury in diabetic rat heart[J].Free Radic Res,2011,45(10):1173-1183.
[31]Maalouf RM,Eid AA,Gorin YC,et al.Nox4-derived reactive oxygen species mediate cardiomyocyte injury in early type 1 diabetes[J].Am J Physiol Cell Physiol,2012,302(3):C597-C604.
[32]Okazaki T,Otani H,Shimazu T,et al.Reversal of inducible nitric oxide synthase uncoupling unmasks tolerance to ischemia/reperfusion injury in the diabetic rat heart[J].J Mol Cell Cardiol,2011,50(3):534-544.
[33]Murphy MP.Induction of mitochondrial ROS production by electrophilic lipids:a new pathway of redox signaling? American journal of physiology[J].Am J Physiol Heart Circ Physiol,2006,290(5):H1754-H1755.
[34]Duncan JG,Fong JL,Medeiros DM,et al.Insulin-resistant heart exhibits a mitochondrial biogenic response driven by the peroxisome proliferator-activated receptor-alpha/PGC-1alpha gene regulatory pathway[J].Circulation,2007,115(7):909-917.
[35]Yamagishi SI,Edelstein D,Du XL,et al.Leptin induces mitochondrial superoxide production and monocyte chemoattractant protein-1 expression in aortic endothelial cells by increasing fatty acid oxidation via protein kinase A[J].J Biol Chem,2001,276(27):25096-25100.
[36]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.